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UNITED STATES OF AMERICA. 



CLINICAL LECTURES 



GOWERS. 



OTHER WORKS 

BY 

W. R. GOWERS, M.D., F.R.S. 



MANUAL OF DISEASES OF THE NERVOUS SYSTEM. 

A Complete Text-book. Second Edition. Revised, Enlarged, and 
in many parts Rewritten. With many new Illustrations. Two Vol- 
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CLINICAL LECTURES 



ON 



DISEASES 



NERVOUS SYSTEM 



DELIVERED AT THE NATIONAL HOSPITAL FOR THE 
PARALYSED AND EPILEPTIC, LONDON. 



BY 

W. R. GOWERS, M.D., F.R.S., 

PHYSICIAN TO THE HOSPITAL; CONSULTING PHYSICIAN TO UNIVERSITY COLLEGE HOS- 
PITAL ; FORMERLY PROFESSOR OF CLINICAL MEDICINE IN 
UNIVERSITY COLLEGE. 



A -5 29 1895 



S^U/Ish^ QjC^ 



PHILADELPHIA : 

P. BLAKISTON, SON & CO., 

IOI2 WALNUT STREET. 
I8 95 . 






, ^ 



1 i> 



Copyright, 1895, by P. Blakiston, Son & Co. 



PRESS OF WM. F. FELL & CC 

1220-24 SANSON! STREET, 

PHILADELPHIA. 



PREFACE. 



The following Lectures have been delivered at the 
National Hospital for the Paralysed and Epileptic. They 
are reprinted from various English medical journals, with 
the exception of two lectures, and for permission to 
reproduce them I am indebted to the J. B. Lippincott 
Company. 



Queen Anne St., London, 
June, 1895. 



W. R. Gowers. 



CONTENTS. 



PAGE 

I. The Principles of Diagnosis of Diseases of the Nervous System, 9 

II. Mistaken Diagnosis, 21 

III. Argyria and Syphilis, 34 

IV. Syphilitic Hemiplegia, 48 

V. Bulbar Paralysis, 71 

VI. Facial Paralysis, 89 

VII. Facial Contraction after Palsy, 108 

VIII. Acute Ascending Myelitis, 119 

IX. Locomotor Ataxy, I, 129 

X. " » II, 143 

XI. The Foot Clonus and its Meaning, 1G3 

XII. Syringo-Myelia, 175 

XIII. The Treatment of Muscular Contraction, 188 

XIV. The Infantile Causes of Epilepsy, I, 197 

XV. " " « " II, 205 

XVI. Neuralgia, 214 

XVII. Lead Palsy, 232 

XVIII. Saturnine Tabes, 242 

XIX. Optic Neuritis, I, ...... 252 

XX. « << II 266 



CLINICAL LECTURES 



Diseases of the Nervous System 



LECTURE I 



SOME GENERAL PRINCIPLES OF THE DIAGNOSIS 
OF DISEASES OF THE NERVOUS SYSTEM. 

Gentlemen: — If we look back over the progress of medical 
science, three epochs of discovery stand out in special 
salience, contrasting, in the steepness of the rise in know- 
ledge they present, with the more gradual progress of other 
branches and of the same subjects at other times. These 
are, first, the revolution in the conception of diseases of the 
heart and circulation which Harvey's great discovery 
entailed; secondly, the penetrating extension of knowledge 
of all the thoracic diseases which was effected by the 
invention of the methods of auscultation and percussion, 
and the discoveries which followed that invention ; and, 
thirdly, the enormous advance in our knowledge of the 
nervous system and its diseases which the last quarter of a 
century has witnessed. This has been largely due to the 
development of microscopical research, in some degree to 

Post-graduate Lecture, Layicet, Feb. 20, 1892. 
2 9 



io PRINCIPLES OF DIAGNOSIS. 

the progress of experiment, but very much to the extra- 
ordinary increase in the capacity for investigation which 
the general progress of science has produced, and to the 
fertile field presented by these diseases for the exercise of 
that faculty. The results of the application of the chemical 
and microscopical investigation to the urine, and the trans- 
forming revelations made through the invention of the 
ophthalmoscope and the laryngoscope, are hardly less 
remarkable, but their range is more limited than those of 
the progress effected during the three great epochs in 
discovery that I have mentioned. The last of these con- 
cerns us in a special manner, because it has taken place in 
our own time and is still in active progress. It is to 
certain consequences of it that I desire to direct your 
attention to-day — consequences that are of the utmost 
importance to the practitioner in his daily work. How 
great, how wide and profound, has been the change that 
our knowledge of diseases of the nervous system has 
undergone cannot, indeed, be realized by all members of 
our profession. A large number of those who studied 
before the change took place have been unable to follow 
the new development of knowledge, — the successive stages 
of which have followed each other with a rapidity almost 
bewildering, and the difficulty has been enhanced by the 
freedom with which investigators have revelled in a novel 
nomenclature, embracing alike the new and the old, in part 
essential, but in still larger measure superfluous. The 
exigencies of practice, with its increasing demand on the 
time and energy of the practitioner, and its unceasing echo 
of the cry (shall I say of a colleague's daughter?) " Give, 
give," has made it often impossible for him to attempt, or, 
attempting to continue, to follow the successive discoveries, 
Without a knowledge of their scientific features he has 
generally found it impracticable to use them, and so he has 
either rested content with that which he learned of old, or 



CHANGED CONDITIONS. II 

has gained a fragmentary knowledge that has served only 
to mislead him. Those, on the other hand, who have 
learned the subject as we have it now, cannot realise the 
change, for they have but one of the terms needed for the 
comparison ; while the large number of practitioners who 
studied medicine during the period in which the change 
was taking place, learned a little of the new and a good 
deal of the old, and acquired a mixture containing many 
incompatibles, with the common consequence that may be 
described in terms of metaphor, not inexact, as " mental 
turbidity." 

To clear your minds and get rid, as far as may be, of all 
that prevents a clear vision of disease, to learn how most 
usefully to see disease through the clearer media, and, 
above all, to see it in such a way as shall enable you to 
treat it with such advantage as is attainable — these, I con- 
ceive, are the objects that bring together here the members 
of this post-graduate course. But I am not sure that the 
students of to-day, or at least many of them, who have 
acquired the latest and fullest knowledge of these diseases, 
have learned, in equal measure, how to use their knowl- 
edge, or are free from the need of that training in method 
which the practitioner feels so keenly. The reason for this, 
or at least the conditions that make it probable, you will 
perceive when I tell you the nature of the difficulty that is 
experienced and the character of the need that is felt. 

Let me, however, first give you an illustration of the 
change that has come over our knowledge of diseases of 
the nervous system during the last quarter of a century. I 
remember, twenty -five years ago, listening to a lecture on 
" chronic spinal meningitis," given by one of the most 
competent teachers of the day, which presented the latest 
and clearest opinions on the subject. The malady, as 
described in that lecture, had no existence. In the case on 
which it was given, the membranes of the spinal cord were 



12 PRINCIPLES OF DIAGNOSIS. 

certainly in a perfectly normal state. The symptoms then 
thought to prove the existence of chronic meningitis are 
now known to depend solely upon changes within the 
spinal cord itself. The pathology had been inferred from 
analogy, but the new means of investigation we have since 
obtained, coupled with the more extensive and precise 
observation which I have mentioned as so salient a feature 
of recent progress, have proved that the analogy was false 
and the malady quite different from that which was sup- 
posed to exist. The symptoms which were then ascribed 
to chronic meningitis are, indeed, now known to manifest 
more than one distinguishable disease. But the chief 
source of practical difficulty is not the mere correction of 
erroneous inference, and the displacement of the work of 
fancy by ascertained fact; it depends on the vast increase 
in our knowledge of the anatomy and physiology of the 
nervous system and on the application of this to disease ; 
it depends, further, on the revelation, effected by micro- 
scopical research, of the extent and variety of degenerative 
processes in all parts of the nervous system. It depends, 
lastly, on our ever-widening perception of so-called 
" functional," really nutritional, diseases for which no 
anatomical cause has yet been discovered, which have been 
distinguished or recognised by means of (i) the increased 
exactness of observation, (2) the aid received through the 
differentiation of processes formerly confused with these, 
but now known to depend on structural change, and (3) 
in consequence of the special indications afforded by the 
discoveries now being made of the vast range of influence 
of toxic agents on the nervous system. Can we wonder, 
then, that our knowledge has been changed, even to the 
point of transformation, and that those familiar only with 
the old should be almost lost in the mazes of the new? 
The practical effect of these changes is to render the cus- 
tomary methods of diagnosis wholly inapplicable to a large 



INADEQUACY OF TYPES, 13 

proportion of cases of disease of the nervous system, to 
render it useless, or more than useless in the case of a large 
number of the nutritional affections that are called " func- 
tional," and of the structural maladies that are called 
" degenerative," as well as many of the maladies that depend 
on the visible and conspicuous changes that are ca'led 
" organic." 

The student has to acquire his knowledge of all diseases 
by the method of ''types," and the same method is em- 
ployed in the practical diagnosis of most other maladies. 
Indeed, in the case of many, no other system of recognis- 
ing the nature of a case could be employed than that of 
observing the correspondence of the symptoms, in charac- 
ter and course, with those of a certain form which is known 
by a special name. But when we turn to the diseases of 
the nervous system that I have indicated, we meet with a 
series of maladies the variety of which is aimost infinite. 
When we consider the various structures comprised in the 
u nervous system," their diversity of function, the extremely 
numerous combinations of structure and function that may 
be deranged at the same time, all mutually acting and re- 
acting to produce the manifestation of disorder ; when we 
consider further the variety of nutritional and degenerative 
processes to which these structures are liable, and also the 
degree and extent to which they are influenced by toxic 
blood states — agencies that we are only beginning to per- 
ceive in their nature and diversity, — we can readily under- 
stand that it not only may be. but that it must be, true 
that the diseases we meet with are so numerous and so 
diverse as entirely to baffle an attempt to range them under 
definite types, that can be designated by definite names. 
But in the series they form, there are here and there aggre- 
gations, as it were, in which the morbid process corre- 
sponds, at least in its chief features, varying only in minor 
points. These we treat as types, and call by names, and 



14 PRINCIPLES OF DIAGNOSIS. 

by them the student learns the general features of the 
classes of disease in which they occur; but they seldom 
stand alone or are marked off by any well-defined bound- 
ary. Intermediate cases connect adjacent groups — cases 
that combine the features of two or several, or present some 
characteristics of one and some of another, and very often 
symptoms that cannot be recognised as pertaining to any 
recognised type. Of these forms, numerous as they are, 
the student for the most part remains ignorant. He has 
enough to do to become acquainted with the more familiar 
groups, and the method by which he learns the features of 
these cannot take in the intermediate varieties. When he 
proceeds to practical work he soon finds himself confronted 
by cases the like of which he has never heard of, and 
which he cannot find described in any text-book of these 
diseases. If he attempts to identify them, to bring them 
under some recognised type, and to give them some definite 
name, he is at once and completely baffled. He is baffled 
of necessity, for the cases belong to no type, and no name 
can be given to them that does not involve more error than 
truth. It cannot be otherwise, for to constitute types and 
assign designations that would include even the chief of 
these varieties would be to multiply both types and names 
beyond the capacity of the human mind to learn, or its 
power to retain. In the case of these diseases, therefore — 
diseases that are so frequent as to make up at least half 
the cases of affections of the nervous system which the 
practitioner has to treat, — the method by which he has 
acquired his knowledge, and by which he is able to deal 
successfully with almost all other classes of disease, fails 
him entirely; and yet in most instances he has nothing to 
put in its place. " The old order changes " ; but it is 
" giving place to new " with a slowness which, at the 
present day, is a source of perplexity and difficulty widely 
felt, and constitutes a really serious obstacle to the practi- 



THE REMEDY. 15 

tioner's work. That it is so — that I am not exaggerating 
the facts — will be, I am convinced, confirmed by most of 
those who bring to their work the earnest and thorough 
spirit which strives to understand the cases that have to be 
treated, which strives after light, and is not content merely 
to deal, in darkness, random strokes. 

What, then, is the remedy ? What new method of 
diagnosis can be adopted ? Happily, there is a means of 
meeting the difficulty, before which its formidable features 
will vanish, and the ever-growing accumulation of facts, the 
ever-increasing variety of definite morbid states of the 
nervous system, however numerous, however complex, 
however unfamiliar, may be dealt with as readily, as surely, 
as the diseases of any other class, or as the affections of the 
nervous system that do correspond to types, and may be 
recognised by such correspondence. Indeed, I had almost 
said that the method I am about to recommend enables 
you to deal with these diseases more readily and more 
surely than the other. At least, it has the advantage of 
placing the practitioner at once in the position needed for 
the adequate and wise treatment of the malady so far as 
such treatment is within our reach. 

The method you should adopt is this : Whenever you 
find yourself in the presence of a case that is not at once 
and completely familiar to you in all its details, forget for 
the time all your types and all your names. Deal with 
the case as one that has never been seen before, and work 
it out as a new problem, sui generis, to be investigated as 
such. Observe each symptom carefully, and consider its 
significance. Then put the several symptoms together, 
and consider the meaning of their combination, especially 
whether there is any one part of the nervous system at 
which disease might cause them all. Lastly, consider the 
way they came on, as indicating the nature of the lesion, 
comparing this with the evidence of their seat, and remem- 



16 PRINCIPLES OF DIAGNOSIS. 

bering also that their character may in itself tell you some- 
thing of their probable nature. When described in the 
abstract, this may seem a lengthy process. It may even 
seem a formidable process. As a rule, it is neither. The 
common symptoms, even those presented by uncommon 
cases, are not numerous, so far as concerns their general 
character and actual nature. The question of localisation 
is only an application of the common physiology of the 
nervous system, of the facts that should be familiar to 
every student, and can be re-learned, if necessary, with 
ease, by every practitioner. All the knowledge needed for 
this method is that which every student gains, or ought to 
gain, in the course of his studies; it is only the mode of 
using the knowledge that is new and has to be acquired. 
But the student should remember the great importance of 
" keeping up " his physiology and anatomy of the nervous 
system, or at least those parts of it which are needed in 
practical work. There is no department of medicine that 
consists more largely of applied physiology and applied 
anatomy than these diseases. For this reason they should 
engage the attention of the student early in his hospital 
work, instead of, as is often the case, being relegated to a 
late period on account of their supposed difficulty — a period 
when his science has got " rusty," or has slowly vanished, 
until even its nomenclature awakens a mere echo from bare 
walls. As a matter of fact, much of the student's hindrance 
is due to this postponement. The application of his knowl- 
edge should be made to retain it. 

But for the successful use of this method it is essential 
that the knowledge, though neither extensive nor profound, 
should be firmly grasped and boldly used. Herein lies the 
chief practical difficulty. Timidity is almost a greater 
hindrance to diagnosis than is ignorance. You must feel 
sure of the meaning of symptoms, you must weigh the 
evidence with care, and then you may and must feel confi- 



FROM SYMPTOMS TO PROCESS. 17 

dent that your conclusion is trustworthy. This confidence 
and boldness can only be acquired by familiarity with the 
process, by observing its use by others, and afterwards 
repeating it for yourselves, thus becoming so familiar with 
the language of disease that you can read it with ease, can 
see at once the meaning of its words, and perceive with 
readiness the significance of its sentences. It is by afford- 
ing an opportunity for this that the attendance on the 
practice, especially the outpatient practice, of special hos- 
pitals, is of peculiar value to the student, whether pre- 
graduate or post-graduate. A series of cases of the same 
class pass before him, in each of which he can observe the 
character of the symptoms and the process of diagnosis, 
and thus he gains, in a short time, a familiarity with the 
features of disease, and a quickness in perceiving their 
meaning, that he could not obtain in a long period of work 
at a general hospital, where such cases are few and far 
between, and the lesson of the one is more than half 
forgotten before another instance comes before him. 

In all this method of dealing with unfamiliar maladies 
there is nothing that is not within easy reach of the 
average student or practitioner. If any difficulty is felt, 
it is only, as in so many subjects, the first step that costs a 
conscious effort. Once learned, the method becomes more 
easy with each repetition, and is acquired the more speed- 
ily if repeated under slightly varying conditions. Soon, 
its steps cease to be consciously felt, and in a short time 
even a student who has been fairly grounded in the ele- 
mentary knowledge, becomes able to use the method with 
precision, and succeeds, in four-fifths of the cases that 
would otherwise baffle him, in arriving at a diagnosis in 
which a physician whose attention has been given for years 
chiefly to these diseases, can find little or nothing to 
change. Note, moreover, that the method indicated is that 
which the most experienced physician has himself to adopt 



18 PRINCIPLES OF DIAGNOSIS. 

in the case of a large proportion of the cases that come or 
are sent to him. So infinitely various are the morbid states 
of the nervous system, so diverse their manifestations, 
that a very large number of the cases seen are practically 
new, even to a man of the largest experience, and if asked 
he has to confess that he has not seen before any case pre- 
cisely similar to, and often not one even approximately 
resembling, that before him. Yet, by employing this 
method, he is able to arrive without difficulty at a diagno- 
sis as sure as when the malady is of a common type. The 
only difference between his work and that of the student is 
that the latter has to adopt the method with scrupulous 
care, in a larger proportion of the cases that he sees. He 
has to deal with a larger number as essentially new pro- 
blems, to be worked out de novo. If he does this, as I 
have said, his errors will be few and rare, and only a small 
proportion of the cases will baffle his efforts. But never 
forget the essentials of the proceeding. Remember that 
you must for the time discard entirely your types and 
names. When you have made your diagnosis in the man- 
ner I have described, then, and then only, may you con- 
sider how far the case corresponds to a type and can be 
called by a familiar or unfamiliar name. 

The last point suggests a common difficulty. The desire 
for a name is strangely strong in the case of the majority 
of patients. Unless their disease is designated, they go 
away unhappy, discontented, distrusting. " But you have 
not told me what is the matter with me " is their parting 
plaint. What are you to do ? In a very large number of 
cases no recognised name can be given to the disease that 
does not involve more error than truth. A few patients 
are sufficiently sensible to endure the knowledge of the fact 
and to be content with it. In the case of most, the 
best plan is to give them a descriptive designation, and to 
write it down, that there may be no mistake, or it will come 



NAMES AND PROCESSES. 19 

back to you some day in altogether altered form, so changed 
that you do not recognise your own production. The 
descriptive designation need not necessarily be short, 
although often it can be, and it then satisfies as much, pro- 
vided the words are unintelligible. " Cephalic dysesthe- 
sias " makes many a sufferer content. " Paroxysmal neural- 
gic pains, due to damage to the third and fourth posterior 
spinal roots, owing to a stationary lesion of the interver- 
tebral articulations," delighted one good woman whom I 
lately saw, and who earnestly desired to know what was 
the matter with her, no doctor, she said, having as yet 
informed her. But always adhere strictly to fact in these 
descriptions, and avoid words that are apt to mislead 
because used in various ways. If you use the term "scle- 
rosis," for instance, the chances are that the patient will 
look up the word in some medical dictionary, will identify 
his malady with insular sclerosis, read, forecast his future, 
and become utterly miserable. 

To sum up in a few words the necessary change. Dis- 
card in the first instance all attempts to identify or to 
name, and try instead to read the malady, tracing the 
symptoms to the seat of their cause, and discerning the 
nature of the morbid process by their character and course. 
The method has the great practical advantage of taking 
you at once to the elements that should guide your treat- 
ment, and of enabling you to treat wisely a case the like 
of which you have never heard of, and a name for which 
you may not know. Mind, I do not say that you need 
adopt this process in every case of disease of the nervous 
system that comes before you. There are many that do 
belong- to familiar types, cases that are characteristic and 
preceived at once to be such — cases of common chorea, 
for instance, of idiopathic epilepsy, many forms of hemi- 
plegia, and the like. But the method is needed in all 
unfamiliar maladies, and in all cases even of familiar aspect 



20 PRINCIPLES OF DIAGNOSIS. 

that present some unusual feature; often, such a feature, 
in the end, is found to indicate that the case merely resem- 
bles superficially that to which it seemed to correspond, 
and is really quite different in nature. 

How real and how extensive is the need for the change 
in method I have described can only be realised by those 
who have to correct the mistakes or supplement the de- 
ficiencies of those who first attempt to make a diagnosis of 
such cases as I have indicated. In many cases a practi- 
tioner candidly confesses his inability. I often receive a 
letter saying, " I cannot make out what is the nature of 
the disease ; I have seen nothing like it before, and I can- 
not find its features described in any text-book." Yet the 
case, as a rule, readily yields to the application of the 
method I have described. More often, however, the prac- 
titioner has endeavored to make a diagnosis by the familiar 
system of types, and has, as it were, forced the case into 
the receptacle that seemed to correspond most nearly to it 
in form, but into which it did not really fit, and has given 
it a corresponding name, more or less erroneous, and often 
ludicrously wrong. I abstain from giving you instances ; 
the statement of the fact will suffice, and examples are so 
numerous that some one would probably find that the cap 
fitted him with unpleasing precision. 

I should like to have given you some instances of the 
working of this method, but for this there is not time. 
You will find it easy and more useful to work out such 
examples for yourselves, beginning with familiar diseases, 
but treating them, for the occasion, as unfamiliar. I hope, 
however, shortly to give you in another lecture a series of 
examples of its use, although not nominally such, by 
describing and analysing some of the more important di- 
agnostic signs, or " diagnostic guide-posts " as we may call 
them. Familiarity with these is of extreme value, and 
most of them will afford illustrations of the use of the 
method I have just described. 



LECTURE II. 
MISTAKEN DIAGNOSIS. 

Gentlemen: — It is always a pleasant thing to be right, but 
it is generally a much more useful thing to be wrong. If 
you are right, all that you do, as a rule, is to confirm your 
previous opinion, your previous habits of reasoning, and 
your previous self-esteem. But if you are wrong you gen- 
erally gain in knowledge and gain perception of the way in 
which your method of diagnosis needs improvement, and 
the influence on self-esteem is not likely to do you harm. 
At least that is my own experience, and I think I have 
observed it confirmed in others. But the result is depend- 
ent on deliberate effort. There is a strong temptation to 
smooth down error, and it is very easy not to gain from it 
its precious lesson. It is more easy to fancy that there is 
some accidental cause for the mistake than frankly to per- 
ceive that it is a fault But if you make a deliberate effort 
to realise and to face in your own mind the mistake you 
have made, to discern its cause, and to employ this percep- 
tion as far as you can to remove the cause and prevent a 
like mistake in the future — if you do this, almost every 
error becomes one of the precious experiences of your 
practical life. 

Yet you will note that I have not said this quite abso- 
lutely. I said it is " generally " more useful to be wrong, 
that " almost" every error is useful. As a matter of fact, 
there are errors you cannot avoid. Beware, however, of 



Post-graduate Lecture, British Medical Journal, July, 1894. 
21 



22 MISTAKEN DIAGNOSIS. 

thinking that any individual instance of error is of that 
character. The chances are great that it is not, that it 
might have been avoided, and they are considerable that it 
will be avoided in the future as a consequence of its occur- 
rence. At least I hope so. 

Still, there are cases in which error is inevitable. I 
should like to mention to you an instance which illustrates 
the conditions on which the relation depends. But this is 
not the chief subject I desire to bring before you. My 
chief object is to seize the opportunity afforded me by the 
courtesy of a private patient and his desire to be useful — 
the opportunity of illustrating avoidable mistakes by an 
example almost perfect in its character, almost unique in 
its features, and seldom equalled in the variety and import- 
ance of the instruction it affords. The case is indeed full 
of important lessons, and it is one the like of which, I ven- 
ture to say, not one of you is likely to have seen before or 
is likely to see again. 

But, first let me say a few words about inevitable errors. 
There is a patient in the hospital at this moment whom I 
cannot show you now, but whose case is an example of 
mistakes that must be. I saw him first about two months 
ago, at the commencement of his illness. I then made a 
diagnosis, of the correctness of which I felt assured, and 
which I am now certain was wrong. Yet if I saw a like 
case to-morrow with the same symptoms, with all the 
knowledge I have gained from this case, I should make 
the same diagnosis, that which proved to be wrong ; and 
the chances are fifty to one, or more, that it would be right. 
Why, in this instance, was it wrong ? Because all diagno- 
sis that rests on reasoning is a matter of probability ; only 
that which is simple observation is certain. The proba- 
bility may be great, or may be only that of a slight pre- 
ponderance of the balance of evidence, but wherever infer- 
ence comes in there is no certainty. Remember that infer- 



THE ROOM FOR ERROR. 23 

ence plays a part which you can discern only by an effort, 
in a large part of diagnosis. You think you observe the 
presence of consolidation of the lung or of pleural effusion. 
You do nothing of the kind. You infer its existence from 
certain physical signs. I remember an incident which illus- 
trates the risk of error thus involved. A skilled physician 
gave orders to his house-physician that a surgeon should 
be called in to tap a chest, one side of which was full of 
fluid. When the surgeon came he took notice of the chest 
before plunging in his trocar, and, being a man of a 
thoroughly scientific mind and used to observation, he was 
struck by the fact that there was no enlargement of the chest. 
Although he was a surgeon, he percussed carefully, and 
found that every other sign of pleural effusion was present 
except enlargement of the side. He declined to tap. A 
little later the patient died, and the lung was found to be a 
solid mass of cancer. That was a case of incomplete 
observation, but it illustrates the fact that even a condition 
like pleural effusion, which you seem to observe, is really 
recognized by complex inference, and if either the process 
of reasoning or the observation is deficient, conclusion may 
be wrong. 

To return now to the case I mentioned. The patient is 
a man of forty-eight years. I saw him a few hours after 
he had been seized with hemiplegia, which had come on in 
a few minutes. Such a sudden onset means a vascular 
lesion, the rupture, or closure of an artery. The onset had 
occurred without any loss of consciousness and without 
prodromata. There was no sign of degeneration or of 
kidney disease. The ophthalmoscopic appearances were 
normal. The hemiplegia was complete; but the entire 
absence of any loss of consciousness made it distinctly 
unlikely to be hemorrhage ; and the facts that there was 
no tension in the pulse, and that there was a perfectly nor- 
mal heart free from hypertrophy, made rupture of a vessel 



24 MISTAKEN DIAGNOSIS. 

still more improbable. The absence, so soon after the 
onset, of any indication of a source of embolism excludes 
embolism — as a practical fact ; and the absence of kidney 
disease made atheroma at that age most improbable. 
When no evidence of any other cause of arterial occlusion 
can be discovered, and there is no condition to cause the 
rare spontaneous thrombosis in a healthy vessel, syphilitic 
arterial disease is probable. It is the condition left by the 
exclusion of others, and it can very seldom be excluded. 
I came, therefore, to the conclusion that it was a case of 
syphilitic arterial disease leading to the sudden formation 
of clot in a branch coming off from the diseased part of the 
artery. But not only could syphilis not be excluded in 
this case ; there was a history of it. The patient was per- 
fectly conscious and able to talk, and gave me a history of 
syphilis more than twenty years ago; an intimate friend, 
moreover, told me of a further history of syphilis as recently 
as eight years ago. Under these circumstances the diag- 
nosis of syphilitic arterial disease and thrombosis was the 
proper diagnosis, and treatment was arranged accordingly. 
The patient was admitted here a short time afterwards, 
and, instead of improving as he should have done, he has 
got worse. By "improving" I mean in the general cere- 
bral symptoms, not necessarily improvement in the hemi- 
plegia. You cannot by treatment restore the lumen of the 
vessel or the tissue destroyed by necrotic softening. The 
treatment is capable only of influencing the condition of 
the wall, and not its consequence. Not only has the hemi- 
plegia continued unchanged, as would be compatible with 
the diagnosis, but the general cerebral symptoms have 
become gravely worse ; his mental state has become 
increasingly dull, weakness of the sixth nerves has devel- 
oped, and, although the optic discs were perfectly normal 
when I saw him, optic neuritis has developed with a 
rapidity and to a degree of intensity that I think I have 



INEVITABLE ERROR. 25 

never seen before. It is certain that he is suffering from a 
tumour of the brain that is not syphilitic, and that in some 
way by pressing an artery the tumour led to the sudden 
formation of clot in it, and the sudden symptoms of the 
arrest of the blood supply in its region. 

Of course, I need hardly add that he was treated by 
iodide of potassium in full doses, and soon afterwards 
mercury was added and pushed just to the degree of 
affecting the gums ; yet not only without improvement, 
but with the contrary. I may incidentally add that the 
mercury was pushed to the degree of affecting the gums 
because, unless you see indications by the gums that there 
is enough mercury in the blood to act upon the tissues, 
the presumption is that the mercury is eliminated so fast 
that there is not enough in the blood to act upon the 
syphilitic tissue. 

Such a combination of symptoms is seldom met with ; 
but we do occasionally meet with a combination of symp- 
toms which illustrates the same rule — that the diagnosis 
which it is right to make is wrong in fact. 

I remember another instance of inevitable error in diag- 
nosis, which I will briefly mention. An old woman, aged 
sixty, was admitted in profound stupor and with indications 
of bilateral hemiplegia and irregular damage to the cranial 
nerves. This state had come on so suddenly we had no 
doubt that there was occlusion of the basilar artery. She 
was sixty, and presented signs of degeneration : therefore 
thrombosis in a branch of an atheromatous artery was 
probable. But she had also mitral constriction, the cardiac 
lesion which of all others is most prone to cause embolism. 
Embolism of the basilar artery, curiously enough, has been 
thought to be impossible, because the artery is larger than 
either of those by which the blood reaches it, but mani- 
festly a plug may pass through one of the vertebrals which 
cannot pass through either of the posterior cerebral arteries, 
3 



26 MISTAKEN DIAGNOSIS. 

which are smaller than the vertebrals. As a matter of fact, 
I have seen a distinct embolus in the anterior extremity 
of the basilar. Therefore embolism was also probable, for 
no age excludes it. The patient died, and was found to 
have syphilitic disease of the basilar, perfectly characteristic. 
This we had no reason to suspect. It is another instance 
of a case in which a correct diagnosis was impossible, and 
error was inevitable. From such cases only the general 
lesson can be learned, that accuracy is occasionally impos- 
sible ; we can only be right in nineteen cases by being 
wrong in the twentieth. It is well to realize this. But 
remember that in practice we have to treat that which is 
only probable as if it were certain. We could not treat 
two-thirds of our cases properly without doing this. But 
always discern the degree of probability, and if the proba- 
bility is low, reduce or modify your treatment so as to do 
as much good as you can, if your opinion is right, without 
certainly doing harm if your opinion is wrong. You will 
find that this principle is applicable to many and various 
contingencies. 

And now we pass to the case which I want especially to 
make the subject of your attention to-day; I should rather 
say "the object," because the attention that I want you to 
give to it is to a considerable extent by the use of your 
own eyes. The patient is a man who first consulted me on 
February 9th, complaining of numbness in his hands and 
feet, with pains, and twitching of the muscles, which were 
increased when he walked. These symptoms were of three 
years' duration and had gradually become worse. They 
began after overwork. He had sharp momentary pains 
in both feet, sometimes in the toes, sometimes in the soles, 
and sometimes in the balls of the feet — not much in the 
legs, and none in the arms. There was no trace of knee- 
jerk ; although there was a little complaint of unsteadiness, 
he could stand, with his eyes shut, fairly well. There was 



AVOIDABLE ERROR. 27 

no incoordination in the hands, and no deficiency in their 
sensitiveness. The pupils acted to light. He had had 
slight brief double vision. There was diminution in sexual 
power but no difficulty in micturition. These symptoms, 
especially the loss of the knee-jerk and the sharp pains, 
afforded a strong presumption of tabes. Inquiry after the 
common antecedent of tabes gave no evidence of it, but did 
not enable it to be absolutely excluded. He came late one 
morning, after I had finished my work, and I had no time 
to examine the state of sensibility upon the legs ; I made a 
note that it was to be examined next time I saw him. I 
generally refuse to see a patient unless there is adequate 
time for investigation, but it is not easy to resist the urgent 
desire for an interview when a patient has come frpm a 
distance. I made the diagnosis of probable tabes, and 
ordered him a mixture containing belladonna, quinine, and 
arsenic. He came again, about five weeks afterwards, say- 
ing that he was about the same. The pains were a little 
less, but the other symptoms were still troublesome. I 
then proceeded to do what I had not been able to do on 
the first interview — to test his sensibility. 

Among the many aphorisms I heard from the lips of the 
greatest bedside teacher whom any living person remem- 
bers, was one that flashed across my mind when, to test 
sensation, the patient's skin was bared. I remember hear- 
ing Sir William Jenner once say : " Gentlemen, more mis- 
takes are made, many more, by not looking than by not 
knowing." To my astonishment, almost to my consterna- 
tion, I saw that the skin presented everywhere the charac- 
teristic pigmentation produced by arsenic. It was a case 
of arsenical poisoning simulating tabes. And I had pre- 
scribed arsenic for him ! Before his illness, and during its 
first year, he was by occupation an oil and colour mer- 
chant, handling papers of various tints, and all sorts of 
pigments, many no doubt containing arsenic. He had also 



28 MISTAKEN DIAGNOSIS. 

during the first year he began to suffer taken a tonic mix- 
ture containing arsenic; but he did not take this long 
enough for it to do more than intensify the poisoning, 
which had no doubt been the result of his occupation. He 
had been exposed for many years ; and it is probable that 
during the two years which elapsed between the develop- 
ment of his symptoms and the time I saw him, that which 
I did others had done. Arsenic had been given him to 
cure his symptoms. 

I need hardly say that I changed the prescription. He 
has not, however, improved. I gave him iodide of potas- 
sium, which seems to have a definite action in eliminating 
arsenic from the system ; but the course of his symptoms 
during the last three months is curious ; they have rather 
increased than lessened, and especially the condition of 
the skin that I will show you in a moment, has become 
more intense. Unless there is some continued cause of 
arsenical poisoning, and we cannot discover it in any way, 
I think the iodide of potassium must have been elimin- 
ating the arsenic from the tissues to such an extent as to 
increase the amount in the blood to a degree that has fur- 
ther irritated the damaged structures. 

Before, however, we examine the skin, let me remind 
you that the nerve symptoms in arsenical poisoning are most 
important. In acute poisoning they are met with after the 
acute symptoms have subsided ; they come on gradually, 
and for a time increase. The arsenic taken in during the 
acute poisoning seems to enter into the nutrition of the 
nerve elements and gradually to derange their function and 
their structure. In chronic poisoning there is a gradual 
interference with function. 

This fact, that arsenic passing into the nerve structures, 
perhaps partly in place of phosphorus, should first gradu- 
ally modify their function, is not surprising. Function 
depends upon the release of force — nerve force — by chem- 



TOXIC INFLUENCE. 29 

ical combinations ; and the amount of nerve energy latent 
in complex compounds, released when similar compounds 
are formed, depends upon the constituents ; so also does 
the readiness with which it is evolved and the kind of 
stimulus that excites the release. But the change in 
nutrition which at first disturbs function in greater degree, 
changes the structure, and leads even to disintegration of 
the substance of the nerve elements. As a fact, this is 
what arsenic and other metallic poisons do. Their action 
presents certain features which you should always bear in 
mind. They reach the structures by the blood. The struc- 
tures on the two sides have bilateral symmetry in intimate 
constitution as in outward form, and that involves a simi- 
lar susceptibility on the two sides. Hence it is that these 
poisons produce symptoms that are bilaterally symmetri- 
cal. 

Moreover, they produce symptoms which are limited 
according to function. There we have a mystery, and yet 
it is a mystery we must recognise as an indication of fact. 
Function must be related to the chemical and molecular 
constitution of the nerve elements. The difference in sus- 
ceptibility to different forms of force must depend on 
atomic constitution and molecular arrangement. We can- 
not conceive that the nerve endings in the skin which pro- 
duce a nerve impulse on the slightest touch are quite the 
same in constitution as those which produce a nerve impulse 
when warmth is applied. We cannot believe that the same 
kind of structure can subserve the susceptibility to the 
massive motion of a touch or to the wave motion, only a 
little less frequent than the waves of light, which consti- 
tutes heat. And that difference, we can understand, is 
equal or greater in the motor and sensory terminal struc- 
tures on which toxic influences for the most part primarily 
act. This enables us to understand why it is that poisons 
act specially upon structures with certain functions, and 



3© MISTAKEN DIAGNOSIS. 

should even act first on one set of sensory nerves and not 
on another set. So we have, from different poisons, differ- 
ent effects upon the nerves, and we have also different 
effects from the same poison, probably dependent on the 
fact that it enters the blood in somewhat different form, or 
with greater or less rapidity, and thus is assimilated by and 
deranges certain structures rather than others. Thus we 
have, from arsenic, palsy of the extensors of the arms and 
feet, as we have from alcohol. We have sometimes a per- 
fect simulation of tabes, ataxy, muscular anaesthesia, and 
loss of knee jerk, in consequence of the preponderant affec- 
tion of the afferent muscle nerves, and sometimes we have 
chiefly sensory cutaneous symptoms, although scarcely 
ever without loss of the knee-jerk. Remember, that loss 
of the knee-jerk only indicates affection of the afferent 
muscle nerves, and that we know that the impairment of 
these nerves has many causes. To all toxic influences 
they seem specially susceptible. 

Hence, I beg you to remember, above all things, as a 
practical rule, that whenever you have bilateral disturbance 
of the peripheral nerves, symmetrical, with a distinct limit- 
ation to function, sensory or motor, it is almost certainly 
due to a blood state. There is reason to believe that the 
degeneration which may appear to constitute an exception 
is really due to a blood poison. Many are the cases in 
which the recognition of that fact will save from grave 
error. 

In the nerve symptoms of this patient there is little more 
for you to observe than I have told you, but if you ascer- 
tain for yourselves the absence of the knee-jerk, the fact 
may be more securely fixed in your mind, and it cannot be 
too surely held. But, as regards the cutaneous symptoms, 
there is a picture for you to study such as you will not see 
again. This arsenical pigmentation is so characteristic that 
the moment I saw it I was sure of its nature, but I never 



ARSENICAL PIGMENTATION. 31 

like my own certainty to be without corroboration if it is 
outside my own special region. So I sent the case to Dr. 
Radcliffe Crocker, and he is also absolutely certain. He 
has seen, he said, one more intense case, and he has kindly 
allowed me to show you a plate from his Atlas, which 
illustrates it. 

I will also read to you his description of the pigmenta- 
tion. But I will add first one more remark. How I have 
become familiar with the pigmentation from arsenic is 
because I have often seen it in the cases of epilepsy. I 
have also seen it in well-marked form, in a lady whose love 
for working on muslins led her to their continuous hand- 
ling, and she preferred aesthetic tints. The result was that 
she began to suffer from pains that were ascribed to gout, 
until there came progressive palsy of the extensor muscles 
of arms and feet. This showed a toxic influence, by the 
symmetry and limitation I have mentioned. Then the 
pigmentation was discerned, although, I believe, chemical 
analysis had already made certain the cause. But the 
troublesome pustular eruption which bromide causes in 
most persons can only be prevented, or kept down to 
insignificant degree, by arsenic. No other drug, no modifi- 
cation of the way or form in which bromide is given, has 
any influence. Some patients are peculiarly prone to the 
rash, and have to take the drug for a long time ; they have 
to take arsenic also. A slight degree of pigmentation is 
often produced in such cases. It has, therefore, several 
times happened to me that I have had to put to the patient 
the two evils, and say, " Which will you have, the spots or 
the pigmentation ? " There is no other help for it ; they 
must have one or the other. They always choose the 
pigmentation. It does not, however, increase to a really 
serious degree, and I have not met with any other symp- 
toms of chronic arsenical poisoning. 

If you observe carefully the skin of this patient, you will 



32 MISTAKEN DIAGNOSIS. 

see that the pigmentation begins as small dots, rounded, 
which coalesce, but leave small rounded areas of unpig- 
mented skin. These appear whiter than normal, perhaps 
only by contrast. The pigmentation is abundant every- 
where, but extreme on the neck, front and back of the 
trunk, arms and thighs. For the most part it appears as a 
pure process, but in many places you will observe small 
round spots of congestion, of the same size, which' suggest 
that, at least when the process is going on actively, con- 
gestion may be the first part of the process. Moreover, in 
the neck, where the skin has been subjected to habitual 
friction, the pigmentation is so intense as to be practically 
continuous, and with it so much congestion is combined as 
to give the skin a reddish or purplish-brown aspect. The 
congestion is also conspicuous on the hands, and there, on 
the palms especially, the spots are attended with distinct 
elevation. Indeed, where the epidermis is thick, there are 
minute raised elevations, at which no indication of conges- 
tion or pigmentation can be discerned. The change in the 
palms, as you have just learned from Dr. Radcliffe 
Crocker's description, may go on to a form of " palmar 
psoriasis." 

The great fact is the pigmentation, at first essentially 
punctate or in small spots. It is that that is so character- 
istic. You will at once understand how important it is to 
be able at once to recognise a sign so distinctive and 
so significant. You cannot note the state too carefully. 
Once firmly fixed in the visual memory, it will not be lost. 
It is seldom easy to retain an image securely from a single 
opportunity of inspection, but this condition is one, I think, 
which you are not likely to mistake when you see it again. 
You may have some other opportunity of observing a 
similar condition. You probably will have such if you 
carefully examine the skin of patients who have been, for 
long, taking arsenic with bromide. But the story of the 



BILATERAL SYMMETRY OF THE RASH. 33 

origin of this patient's illness suggests that a careful inspec- 
tion of the skin of a number of men employed in shops 
where paints and papers are sold might afford an inquiring 
student opportunities of observing the pigmentation, which 
would be beneficial not to himself alone. It is certain that 
the change in the skin may long precede any other 
symptom. 

Having helped you so far, gentlemen, I must now ask 
you to help yourselves. Observe, also, what I have not 
mentioned, the bilateral symmetry of the rash, a feature 
that you will recognise, from what I have said, to be 
inevitable. Connect it with the bilateral pains and loss of 
knee-jerk, and fix these features of limitation and symmetry 
in your minds in association with the toxic cause. For a 
moment, indeed, forget what the cause here is, forget the 
precise character of the symptoms, in order that the general 
facts of combined functional limitation and bilateral sym- 
metry may stand out more clearly in your view as land- 
marks which, when and wherever they are seen, will 
always guide you surely. 



LECTURE III. 
ARGYRIA AND SYPHILIS. 

Gentlemen : — It is the duty of a clinical teacher to bring- 
out of his treasury things old and new. He is constantly 
under some temptation to present ideas that are new, 
because they possess more intrinsic interest, although it is 
generally more useful to give those that are old. Truth 
and novelty are by no means necessarily associated, although 
a familiar phrase which suggests mutual exclusiveness goes 
too far. Nevertheless, it is well for a teacher, if he can, to 
resist the attraction of the new, and it is always unwise for 
him to hesitate to inculcate that which is old merely 
because it is old. Years ago, when I was engaged in giv- 
ing the elements of clinical instruction to students who 
were beginning their practical studies, I used to paraphrase 
the saying of Demosthenes regarding oratory and maintain 
that the first thing in learning is repetition, the second repe- 
tition, and the third repetition. A teacher should remember 
that to neglect to repeat is an unpardonable sin. There is 
an unpardonable sin of the student ; in fact, it was the re- 
membrance of this that made me use the term. It is not 
my own idea. Years ago Sir William Jenner used to say 
to us (and whatever Sir William Jenner said may be a priori 
regared ascertain) that the unpardonable sin of the student 
was to say " Yes " when he ought to say " No " — to say 
that he heard a thing, that he felt a thing, that he under- 
stood a thing — when he did not. 

For you this lesson is probably useless, because you have 

British Medical Journal, December I, 1894. 
34 



AN AID TO PROGNOSIS. 35 

all passed the stage at which it is needed. But it may not 
be too late to remember that it is a mistake to shrink from 
unattractive repetition. Consider — what are we all learn- 
ing, or should be learning, on this point, from our great 
Teacher? What does Disease impress upon us ? Disease is 
forever repeating to us the same things. All the more 
important laws and rules are ever being pressed upon us, 
in varied tone, by varied emphasis, or in varying language, 
but ever repeated. No repetition should be or will be use- 
less to us if we take the requisite pains, and are not 
deterred by weariness from striving to discern the lessons 
that seem the same, but present always an important dif- 
ference ; and no repetition of fact to us by disease is ever 
superfluous, unless we will to make it so. 

Yet the teacher is, as a rule, compelled to take as a 
subject for his instruction some fresh illustration of disease. 
It is seldom that he has an opportunity of taking that 
which is old. When he can it is well for him to do so, for 
more than one reason. All old cases afford an opportunity 
of observing the changes in disease, and the effects that 
time permits. The question which ever presses on us when 
we meet with disease in its active stage is this : What will 
be the future ; what will be the result ? We can only learn 
to look forward by taking every opportunity of looking 
back. We cannot combine in our observation the future 
and the present. Our own experience and that of others 
may enable us to guess something of the future from the 
present ; but every personal observation that increases our 
ability to forecast, everything that helps to make the guess 
more than a guess, is important. This help can only be 
obtained when the future has changed to the present. We 
can realise the past, and discern its relation to the future 
when that which was future has come. We cannot, with 
the same confidence, realise the unknown future and apply 
it to the present. Some of you may remember the lines 



36 ARGYRIA AND SYPHILIS. 

which come to my mind — lines by a poet who is almost 
forgotten now, although his name should live in the mem- 
ory of medical readers. Sidney Dobell wrote in one of 
his sonnets, in which sadness touches softly — 

" And when the now is then, 
And when the then is now." 

If the " then " is in the past, we can, by fancy, make it 
" now ; " the " then " is clearly seen, for it is now a fact, and 
we can thus gain some secure experience in prognosis. 

I show you to-day a patient who presents an opportunity 
of illustrating the present by the past, and by a past in 
itself most instructive, such as seldom occurs to a teacher. 
I imagine it is almost a unique opportunity for a teacher to 
be able to take as a subject a patient who has been under 
his observation for a quarter of a century. That is the case 
here, and I am glad to have so unusual an opportunity in 
beginning again the series of our Wednesday lectures. It 
is nearly, if not quite, twenty-five years since this patient 
was under treatment in the wards of the hospital in the 
acute stage of his affection. 

Did you notice him as he came into the room ? If you 
did not, you should have done so. One of the habits to be 
acquired, and never omitted, is to observe a patient as he 
enters the room ; to note his aspect and his gait. If you 
did so, you would have seen that he seemed lame, and you 
may have been struck by that which must strike you now — 
an unusual tint of his face. Those two things are import- 
ant. They are, indeed, connected, but in a way that is 
rather curious than instructive. It is, indeed, so curious 
that I cannot resist the temptation of telling you the story 
it involves. 

The patient came here in 1870, with symptoms of a cere- 
bral tumour, of rather rapid onset for such a morbid process. 
The symptoms had reached to a considerable degree in 



A PATIENT OF LONG-STANDING. 37 

about two months. The patient presented indications of a 
sub-chronic local cerebral lesion, with headache and optic 
neuritis. These two general cerebral symptoms with the 
onset indicate that the local process is a growth. More- 
over, there was a history of active syphilis ; and we know 
that whenever we have evidence of a local growth of rather 
rapid course in the subject of syphilis the probability is very 
great that the growth is syphilitic. They are much less if 
the growth is very chronic, and this point is important. 

The patient was treated according to the diagnosis. He 
was not under my care, although he was under my con- 
stant observation ; I was then Medical Registrar to the 
Hospital, and he was under the care of Dr. Hughlings 
Jackson, from whom it was my privilege to learn many 
lessons of ever-increasing value, and not the least important 
were connected with this case. After the patient's dis- 
charge from the hospital he was under my care as an out- 
patient, of late years only seen occasionally, chiefly for the 
benefit he is always ready to give to others as an illus- 
tration. 

When he first came to the hospital he was lame, as he is 
now, and he presented the complexion aspect you see, but 
in a greater degree. An inquiry into his history showed 
that two years previously he had been an in-patient at a 
general hospital, under the care of a physician then well 
known, who has now been dead many years. The symp- 
toms he then presented were those of a small syphilitic 
growth pressing on one side of the spinal cord, and causing 
effects that we now know to be very characteristic. For 
those symptoms he was treated with nitrate of silver, and 
his skin acquired the aspect which it has never lost. When 
he came here he had improved, and I think, for several 
reasons : it is exceedingly likely that after the nitrate of 
silver had been given for a considerable time, without other 
result, mercury was substituted. At any rate, the affection 



3$ ARGYRIA AND SYPHILIS. 

of the leg ceased to increase, improved somewhat, and then 
became stationary, and when he came to this hospital its 
state was much as it is now. with due allowance for the 
effect of the fresh trouble which brought him to us. 

In connection with his case there is a little story which 
I cannot resist the temptation of telling you, especially 
since the patient here can correct me if I am wrong. Per- 
haps it is a little beyond the proper subject of a lecture, 
but I dare say. gentlemen, you will not be strict. The 
patient suffered from severe headache, optic neuritis, and 
signs of a local cerebral lesion in one cerebral hemisphere, 
of subacute onset. It was certainly a quickly growing 
tumor, and almost certainly syphilitic. Thus the case was 
most instructive. In 1S70. as you know, not quite so much 
was known of optic neuritis as is now known, and he was 
shown to a good many visitors. The interest, too, was 
not lessened bv the indications of ars^-ria — the staining of 
the face from nitrate of silver for a morbid process in the 
spinal cord similar to that which in the brain lessened with 
extreme rapidity under iodide of potassium. 

Great care and caution were taken in all that was said in 
his presence. I can even now remember the scrupulous 
circumlocutory care adopted to guard against any :ercep- 
tion, on his part, of what was thought about his previous 
treatment. But the man possesses a considerable amount 
of intelligence, and he picked up too much information, 
although he gave us no indication of the fact. The symp- 
toms rapidly subsided. On the morning after his discharge 
he paid a visit to the physician under whose care he had 
been, and from whom he had received the silver. He 
obtained an interview with the doctor. The result of that 
visit was, I am certain, to improve the therapeutical knowl- 
edge of the physician, and I have also no doubt that the 
result was very much to the advantage of any other patient 
who subsequently came under the care of that physician 



AN ILLUSTRATION OF ARGYRIA. 39 

for a similar affection. But the immediate result was a 
considerable disturbance of equanimity. The patient was 
wise enough to content himself with thus conveying 
instruction. He might, I think, have gone further; but 
I doubt whether even a speculative lawyer would have 
induced him to do so, for he is, after all, a reasonable 
fellow. I think one cannot find very much fault with the 
lesson, or even, considering all things, with the way in 
which it was given. 

[Dr. Gowers here turned to the patient and asked if the 
account given was substantially correct. The reply was: 
" Yes, sir ; it's all right. I jacketed him."] 

I imagine that it is very likely that some of you have 
never seen the tint of argyria. It is less commonly met 
with now than formerly, because nitrate of silver is less 
frequently given, and when it is given, it is given with 
more care. It will therefore be wise for you to note very 
carefully the aspect of this patient. The tint is rather less 
than it was, but it persists, and it will persist as long as he 
lives. There is not now a black line at the edge of the 
crums ; I think it was there formerlv. We have been 
unable to find the old notes of the case, but all the essen- 
tial facts are adequately impressed upon my memory. I 
have only myself seen about four cases of staining from 
nitrate of silver. This is one. Two were in cases of epi- 
leptics, for which it was, as you know, once a reputed 
specific. It was held in very high esteem by some persons 
in what have been called the " pre-bromidic days." Both 
the patients I saw, who had been stained with nitrate of 
silver for epilepsy, were still patients here for the persisting 
disease, and therefore my own observation did not lead me 
to entertain a very high opinion of its value. 

The fourth case is instructive because it was due to the 
use of nitrate of silver for the good it can unquestionably 
do in gastric affections, especially when pain occurs before 



40 ARGYRIA AND SYPHILIS. 

meals, that is, when it coincides with the absence of food. 
Although in cocaine we have an agent which seldom fails 
under these conditions, it is not unlikely that this use of 
silver will again increase. It may be then that the lesson 
this case gives may be again needed. A doctor, an 
esteemed practitioner in a suburb of London, gave his 
brother, who suffered much gastric pain, a "dinner pill," 
to be taken before food every day ; it contained some oxide 
of silver. A year or two after, when shooting together in 
Scotland, the doctor became uneasy at his brother's cya- 
notic aspect. He watched him closely, and at last asked 
him : " Do not you get short of breath as you go up hill ?" 
But there was no shortness of breath, and the doctor did 
not think anything more about it. Six months later, the 
tint had increased, and it suddenly flashed across the doc- 
tor's mind, " Why, it must be silver ; there is that pill ! " 
He turned to his brother and said, " Have you been taking 
those pills ever since I first gave them ?" " Yes," was the 
answer, " I have been taking them ever since, and am 
still." By this time his face had become deeply tinted. 
The line on the gums was most distinct. Although they 
were at once stopped, other remarkable troubles came on. 
There were no signs of lead poisoning, no colic, and no 
conceivable source of saturnism, but the patient developed 
wrist-drop, just like the wrist-drop of lead poisoning, and 
also developed the gout that is so often due to lead, and he 
developed the albuminuria associated with it. Silver does 
cause palsy in animals ; we know how many metals may 
cause the symmetrical extensor palsy, and I think there 
can be no doubt that in this case the palsy of the extensors 
of the arms was due to the silver, although the case, as far 
as I know, in that respect, is unique. The sequel of the 
symptom, I may add incidentally, was most illogical. The 
patient died two years later, but he died from cancer. With 
adequate mischief to terminate life by intelligible effects, he 



ORGANIC HEMIANESTHESIA. 41 

died from something altogether different, which is an illus- 
tration of the limits there are to our power of inference and 
forecast. 

Let us turn to the patient before us. He left the hospital 
with some symptoms remaining from the disease in the 
brain ; these had become stationary, and they have persisted 
ever since. I said he had symptoms of a local cerebral 
lesion. These symptoms were slight left-sided weakness, 
left hemianaesthesia to all forms of sensation up to the mid- 
dle line, head, limbs, and trunk ; considerable diminution 
of the special senses on that side — taste and hearing, while 
vision was affected as hemianopia. Of smell I am not sure. 
If impaired, the defect did not persist, and his present re- 
collection is that it was normal. The hemianopia was at 
first complete. 

Leaving smell out of consideration for the moment, you 
know that left-side hemianaesthesia, involving the skin and 
the special sensories, is the characteristic of what is called 
hysterical hemianaesthesia, a functional condition of the 
existence and reality of which there can be no doubt. Nor 
can there be any doubt of its practical independence of the 
patient's will. There was the difference, however, in this 
condition from the hysterical form — that in the latter the 
affection of vision is a diminution in the whole field of 
vision. There is a considerable general diminution in the 
field of the opposite eye, and a slighter similar diminution 
in the field on the other side — that is, the side of the central 
hemisphere involved. In this case, however, there was 
hemianopia on the opposite side. That is the great differ- 
ence between this form of hemianaesthesia, that which is 
due to organic disease, and that due to a functional affection. 
Nevertheless, there is evidence to show that " crossed am- 
blyopia," dimness of vision, with general restriction of the 
field, greater on the opposite or " crossed " side to the 
affected hemisphere, may occur from organic disease as it 



42 ARGYRIA AND SYPHILIS. 

does from hysteria. But the reason why an organic lesion 
generally causes hemianopia is this. The lesion is generally 
at one place, at the region which Charcot has called the 
" sensory crossway," at the posterior extremity of the inter- 
nal capsule between the optic thalamus and the end of the 
lenticular nucleus. 

The sensory fibres from the skin, from the head, and 
limbs run in the posterior third of the hinder limb of the 
capsule. The optic tract conveys impressions to that region, 
the fibres from the same-named half of each retina conduct- 
ing impressions from the opposite half of each field of 
vision pass to it. Thus the impressions passing to this 
hemisphere are those from the side on which the motor 
processes act on the limb. Each half of the brain receives 
impressions from the side on which it moves the limbs. 

The fibres from the optic tract that subserve vision pass 
into the white substance of the occipital lobe. They prob- 
ably have an intermediate station in the posterior extremity 
of the optic thalamus. But I need not now dwell on this. 
Whether they pass from the thalamus or directly from the 
tract they must pass close to the extremity of the capsule, 
close to the sensory fibres from the skin. Thus disease here 
causes hemianopia and cutaneous anaesthesia. But it also 
causes loss of taste and hearing. This is so well established 
that we are sure that the paths for these sensory impres- 
sions pass by this region. Moreover, there are cases on 
record of an affection of smell from disease of this region, 
but the point needs further evidence, and as this case has 
no definite bearing on it, I will pass it by. But I must 
emphasise the fact that cases of organic disease have been 
met with which cause symptoms resembling closely the 
hysterical form of hemianesthesia. The latter we must 
ascribe to an inhibition of the sensory structures in one 
hemisphere. In the cases of organic disease that cause 
similar symptoms, extensive disease has existed on the 



VISUAL DEFECTS. 43 

convexity of the hemisphere, so extensive that we can- 
not infer more than that it is in the convexity of each 
hemisphere that the impressions are represented which 
come from all the special senses of the opposite side, in- 
cluding smell. In these cases there is " crossed amblyopia." 
But, beyond recognising the fact, you need not now con- 
sider the condition. Our subject is the sensory effect of 
disease that causes vision to suffer, as " hemianopia." Half- 
sight is lost with the other senses if the disease is in the 
tract, the sensory-crossway, or the half-vision centre in the 
occipital lobe. This was the combination the patient pre- 
sented. The association of hemianopia and impairment of 
the general and special senses on the same side proved 
that the disease was situated where all the paths are in 
contiguity — that is, at the place I have mentioned. Be- 
yond this the paths diverge, so that the combination can 
be produced only by disease invading the whole cortex of 
the convex surface, including the occipital lobe, and then 
there is the crossed amblyopia as well as the hemianopia. 
There is restriction of the field as well as half loss. We 
may now turn to the symptoms the patient still presents, 
the permanent residue of those caused by the active disease. 
Persisting as it has for the past quarter of a century, we 
may actually expect it to persist for the next quarter of a 
century, which is probably about as long as the patient may 
be expected to live. A slight defect of taste and of hear- 
ing is still distinct. In the limbs there is still imperfect 
sensation. 

The defect in vision that still persists is particularly in- 
structive. You can easily verify it for yourselves. In one 
pair of charts before you, you see first the fields of vision, 
as they were nine and a-half years ago — that is to say, 
about fifteen years after he came for treatment — and the 
others present the condition that exists at present. The 
two are practically identical. In each there is a loss of 



44 ARGYRTA AND SYPHILIS. 

the left lower quadrant. At first the whole half field was 
lost, up to the middle line ; but the upper part recovered 
slowly, so as to leave the loss confined to the area you 
see. In it there are points that it will be instructive to 
you to note. The loss stops short of the fixing point. 
That, as you may know, is a characteristic of all forms of 
hemianopia, at any rate of lateral hemianopia. I show 
you another diagram, in which the loss is of the whole 
half field, in which the feature is well shown. The blind 
area reaches the middle line, above and also below ; but 
the dividing line between sight and blindness curves round 
the fixing point, so as to leave an area of vision. This is 
the rule — I believe invariable. Around the fixing point 
there is vision on the blind as well as the seeing side. I 
believe that apparent exceptions are due to imperfect 
observation — imperfect almost of necessity, because the 
area of sight around the fixing point varies, and special 
means are needed to ascertain it when it is small in ex- 
tent. The explanation of it is that from the region just 
around the macula lutea fibres pass by each optic tract to 
each hemisphere. Hence, disease of either optic tract, 
while causing hemianopia, does not cause loss in that 
small region from which the fibres go to each tract. It 
may have occurred to you that if fibres pass to each optic 
tract, disease of either should lessen the function of the 
whole of the region, although causing no absolute loss on 
either side. It is so. If you test minutely the central 
area of vision of a patient with hemianopia you will find 
that, although the region round about the fixing point is 
spared, the acuity of vision in it is definitely reduced. 

Note also another point of significance. There is but 
little restriction in the general field of vision. The very 
slight diminution in the general area of the peripheral 
parts of the fields is not greater than can be accounted for 
by a dark day, or even by an individual variation ; yet 



PERSISTENCE OF SYPHILITIC SYMPTOMS. 45 

note how different is the extent of the remaining half 
fields in the other chart I show you. Notice the remark- 
able restriction of field, and that it is much greater in the 
eye on the side of the half loss — that is, the right half of 
each field being lost, the remaining part of the right field 
is much smaller than the left. I must not, however, 
allude to this to-day beyond asking you to remember it in 
connection with " crossed amblyopia." 

And now, gentlemen, in conclusion, I have to impress 
upon you one practical lesson which this patient gives us, 
and which he gives as an old patient. It is the persis- 
tence, in some degree, of the effects of syphilitic disease, 
and that in spite of the fact that the patient was treated 
thoroughly, a few weeks after the development of the 
symptoms — which is as promptly as most patients are 
treated. It was manifestly adequate, for the urgent gen- 
eral symptoms, headache and optic neuritis, began to lessen 
within a week, and in the course of a few weeks all the 
acute symptoms had passed away, and the local symptoms 
were rapidly improving, the loss of power had become 
trifling, the hemianesthesia gradually became partial in- 
stead of complete. Yet some of these symptoms have 
never quite passed away. 

The optic neuritis when he came in was considerable, 
but not extreme. The whole disc was obscured by a 
swelling of moderate prominence and considerable vascu- 
larity, yet the acuity of vision was perfect. The inflam- 
mation was not sufficient in itself to have involved the 
nerve fibres so as to impair sight by the process of inflam- 
mation in them, nor was it sufficient to produce new 
inflammatory products sufficient to damage the fibres by 
their cicatricial contraction. Those are the two ways in 
which sight suffers from the neuritis. In those days 
ophthalmic surgeons generally refused to believe that 
considerable neuritis could exist with perfect vision. The 



46 ARGYRIA AND SYPHILIS. 

scepticism was chiefly dispelled by Dr. Hughlings Jackson, 
and I think that this patient was one of the cases by which 
the dissipation was effected. Fortunately the treatment 
was early enough to remove the neuritis before grave 
damage was done to the fibres. His sight has remained 
good so far as acuity of vision is concerned, and his optic 
discs now present such a perfectly normal aspect that you 
would not suspect they had ever been inflamed. I should 
advise you to examine them carefully, because it is very 
seldom that you have an opportunity of seeing optic discs 
which are known to have been the seat of inflammation, 
and which now present no indication of it, and especially 
discs that were inflamed long; ago. 

The practical lesson that I mentioned, and which I should 
like you to take away, is this : The idea is not yet extinct 
that all syphilitic disease will yield to treatment, and that 
if only the symptoms are certainly due to syphilis they can 
be cured. Probably you know well as regards the nervous 
system how erroneous that idea is. You know that a 
syphilitic ulcer of the skin will, and must, leave a scar 
which nothing can remove. It destroys the tissue of the 
skin, and that tissue of the skin being destroyed is never 
replaced by structure which is like the old skin in aspect 
and function. So it is with the brain. If there is absolute 
destruction of tissue by a syphilitic process, that tissue 
cannot be renewed, and is not renewed ; the symptoms 
dependent on its destruction will not pass away unless 
other parts of the brain can compensate for their loss. 
Remember that, as I have often said, the symptoms of a 
local lesion are never due directly to the syphilitic process. 
In true syphilitic affections, those which can be removed by 
iodide of potassium and by mercury, the syphilitic process 
is altogether outside the nerve elements themselves. These 
suffer secondarily, as they would from any other process 
of a similar general character. They suffer from compres- 



IMPORTANT LESSONS EMPHASISED. 47 

sion by such a syphilitic gumma as this patient had, as 
they would from any other tumour. They suffer somewhat 
from the inflammation adjacent to any rapid growth, but 
this is usually simple inflammation with no necessary 
specific element. Through these processes they undergo 
damage and destruction, and no removal of the growth can 
do more than permit the recovery of those structures which 
are so little damaged that their recovery is possible. In 
the patient before you the damaged structures recovered. 
Destruction, of necessity, persisted, and the effects of the 
loss of tissue remain, where no compensation could be 
effected. That is the case with the half-vision centre and 
the fibres that carry impulses to it. Destruction of these 
causes destruction of the function and lasting loss. We 
have in the quadrantic loss of the fields of vision a proof of 
this fact. We have in it also evidence of the equally 
important fact that the effects of syphilis are often far more 
than that to which the term "syphilitic " can be applied. 
If you learn from this to look at a process with the 
imagination, that is as important in practice as in science ; 
if you learn to discern the elements on which symptoms 
depend, and to be cautious in your prognosis in such cases 
of syphilitic disease ; if you learn also the lessons the 
patient teaches regarding silver as well as syphilis, you 
will not have wasted your hour here to-day. 



LECTURE IV. 
SYPHILITIC HEMIPLEGIA. 

Gentlemen : — You have probably long since become con- 
versant with the truth that the most important part of 
learning is repetition. If this be true in the process of 
acquiring knowledge, it can hardly be otherwise in the 
process of imparting it. In conveying, as well as in receiv- 
ing, instruction it is essential that the knowledge which has 
to be securely retained should be impressed upon the 
learner as often as opportunities permit. It may not be the 
most attractive element in the process, but another lesson 
which you have doubtless by this time learnt only too well 
is that the attractive is seldom the most useful, or the useful 
the most attractive. 

Last week we examined an example of a rare disease 
and considered what is known of its nature, the process of 
its diagnosis, and the possibilities of its treatment. You 
had to hear of much that is conjectured but not proved, 
and of much that is still mysterious. To-day I propose to 
show you a patient who is suffering from a common malady 
whose symptoms can be traced to their source with reason- 
able certainty by means of the methods which must often 
have come under your notice, but which you will have to 
apply so frequently that they can scarcely be too often 
reconsidered. This is an advantage, not only for the sake 
of the repetition, but because no two cases of disease pre- 
sent precisely the same features in state and history ; and 
in every case you will meet with one or more elements 

International Med. Mag., October, 1893. 
48 



LOCATING THE HEMIPLEGIA. 49 

with which in that combination you are not familiar, and 
only experience in applying the processes of reasoning to 
the facts observed will enable you to place them in their 
proper relation and make them yield you the guidance 
you require. 

The patient before you is suffering from hemiplegia, from 
paralysis of the right side. Common as hemiplegia is, one 
feature of this case should at once strike you as somewhat 
unusual. The forms of hemiplegia with which you are 
chiefly familiar have been in persons of advanced life, but 
this patient is only twenty-five years of age, and the affec- 
tion has only existed for two months. Probably you have 
seen some cases of the affection in young persons, but not 
many in whom it has come on at this period of life. 

If you note the power of movement which he possesses, 
you will see that he can move the upper part of the face as 
well on the right side as on the left, but he cannot move 
the lower part of the face so well. His tongue is not 
affected; it is protruded straight. His arm is feeble; he 
can move all parts of it, but cannot exert force with any 
part, and the movements of the hand are not quite steady. 
His leg is also weak, so that he can only just manage to 
walk alone. 

When you are accustomed to cases of the kind, your first 
thought will probably be, and, indeed, may reasonably be, 
What is the nature of the lesion ? and your second, What is 
its place? This is to put the chief elements in the diagnosis 
in the relative position which they occupy as regards the 
practical questions of prognosis and treatment as regards 
the interest of the patient. But the strictly logical order is 
to consider first where the lesion is, and, secondly, what is 
its nature. It is best to adopt this order in the case of dis- 
eases of the spinal cord, and we will adopt it now ; but in 
the case of diseases of the brain there is no real inconven- 
ience in considering first the nature of the affection. 
5 



50 SYPHILITIC HEMIPLEGIA. 

The first diagnostic indications should be familiar to you. 
Paralysis of the face, arm, and leg on the same side must 
be the result of a lesion above the middle of the pons. 
Here the motor path for the face leaves that for the limbs 
and crosses over the middle line, and in disease below this 
point the face escapes or is affected on the side opposite to 
the limbs. Disease in the upper half of the pons often in- 
volves the fifth nerve on the side of the lesion, — that is, 
the side opposite to the paralysis of the limbs. Very rarely 
it does not, and the palsy resembles that which is due to 
disease higher up the motor path ; but such exceptional 
cases, which are not met with in more than one case in a 
hundred, may be put out of consideration. Disease of the 
crus involves the third nerve on the side of the lesion, and 
opposite to the paralysis of the limbs. When these indi- 
cations of involvement of the cranial nerves are absent you 
may safely conclude that the lesion is within the cerebral 
hemisphere. But where? It must be in some place in 
which it can damage the fibres that conduct the motor im- 
pulses, or the centres from which the fibres proceed and in 
which the impulses are generated. Experience shows us 
that there are three regions in which lesions are prone to 
occur and in which they may cause this effect. One is the 
central ganglia, the second the white substance, the third 
the gray cortex. 

Lesions in the white substance of the hemisphere are 
not common. Moreover, if they are near the cortex the 
effects they produce are commonly very similar to those of 
disease which is in the cortex. If, on the other hand, they 
are near the central ganglia, the symptoms which they 
cause are like those that are produced by disease of the 
latter. Hence, for practical purposes, we may leave them 
out of consideration, and, indeed, we are compelled to do 
so, except in rare cases in which the diagnosis depends 
upon indications too complex to be included in a general 



LESION IN THE CENTRAL GANGLIA. 51 

outline of the subject, such as I am now attempting to give 
you. Thus our problem is limited to the distinction of 
disease in the two remaining situations. I have spoken of 
the central ganglia, but a lesion there does not cause hemi- 
plegia by its effect on the ganglia themselves. Even ex- 
tensive destruction of their gray matter produces no paraly- 
sis. The hemiplegia depends upon the interference with 
the narrow tract of white fibres which passes between them, 
and which, bounding as it does the lenticular nucleus on 
the inner side, is spoken of as the internal capsule. When 
the middle of this and the part behind the middle are dis- 
eased, hemiplegia is produced, for the fibres here are those 
which conduct the voluntary impulses from the cortex from 
its " motor " or " central " region. This, as you well know, 
is the part whence the motor impulses leave the cortex, 
and disease in this region causes hemiplegia like that which 
is produced by disease of the internal capsule. 

How can we tell in which of these two situations the 
lesion is ? First, by the fact that cortical disease means 
damage to nerve-cells, and that damage to motor nerve- 
cells is apt to be attended by the spontaneous action which 
is manifested by convulsion, while disease of the central 
ganglia does not cause convulsion. Secondly, from the 
fact that the close approximation of the fibres for the face, 
arm, and leg in the internal capsule and the disassociation 
of the centres in the cortex make it common for all parts 
of one side to be affected in capsular, and for only some 
parts of the side to suffer in cortical, disease. But this is 
not an absolute rule. All parts of the motor region may 
be affected in the cortex, and only some parts of the motor 
part in the capsule. But it must be a very small lesion in 
the latter to produce only a partial effect, and a severe lesion 
in the former to produce a complete effect. Here we 
have the indication of a guiding distinction. You must 
consider the significance of the distribution of the palsy in 



52 SYPHILITIC HEMIPLEGIA. 

connection with its extent. In this case all parts of the 
face, arm, and leg have suffered, but only in moderate 
degree. Hence we may assume that the lesion was not 
severe, and the distribution, therefore, is strongly in favor 
of the lesion being in the region of the central ganglia. 
The tongue, indeed, has escaped, but this is not surprising 
if, as we perceive is probable, the lesion is incomplete. 
The diagnosis is further supported by the fact that the 
patient did not suffer from convulsions at the onset, and 
has not suffered from them since. If such convulsions had 
occurred, or if there were absolute paralysis of the arm 
and no affection of the face, we should be justified in con- 
cluding that the disease was in the cortex. You may thus 
perceive the chief points that must be taken into consider- 
ation in this point of localisation, and you will find that 
they will afford trustworthy guidance in a majority of the 
cases which come under your notice. 

We may accordingly conclude with reasonable confi- 
dence that the symptoms are due to a lesion in the cen- 
tral nuclei, which has caused the hemiplegia by the damage, 
extensive but moderate in degree, to the fibres of the 
internal capsule. In scanning the brain of persons who 
have suffered from transient hemiplegia some time before, 
you may sometimes see nerve-fibres passing almost intact 
through an area of disease which involves the gray matter 
on each side of them, although the gray tint of the fibres 
on the surface of the layer shows that many of them have 
suffered structural damage, although there may not have 
been actual interruption. 

The next question is, What is the nature of the disease? 
This is, indeed, a double question, for we have to consider 
first what is the lesion which has caused the symptoms, and 
next on what pathological process does that lesion depend. 
Several features of the disease are commonly available for 
ascertaining the nature of the lesion, but of these one 



PROGNOSTIC VALUE OF MODE OF ONSET. 53 

exceeds all the rest in its importance in the readiness with 
which it is ascertained and with which it is applied, and the 
security of the information which it affords. It is the 
mode of onset. Each morbid process develops in a certain 
time, which varies, it is true, but varies only between limits, 
and these limits constitute our guide. The onset of the 
symptoms is that which manifests the rate of development 
of the process. For practical purposes, within which the 
majority of the cases will be found to come, three different 
modes of onset are to be recognised, — the chronic, the 
acute, the sudden. I need not amplify the words. A 
chronic onset means a tumor or sclerosis, an acute onset 
inflammation, a sudden onset a vascular lesion. Fix, I beg 
you, the last axiom firmly in your minds. You may rely 
upon it absolutely, and you will find the value of its guid- 
ance, not seldom, when you are perplexed by the intricate 
maze of discordant indications. Of course, I am speaking 
only of organic disease, and of these it is always true that 
a sudden onset means a vascular lesion. It means rupture 
causing hemorrhage, or obstruction causing, first, anaemia, 
and, unless at once compensated by a collateral flow, 
necrotic softening. 

What was the mode of onset, what was the time occu- 
pied by the onset, of the symptoms from which this patient 
is suffering ? If you put the question to him he will tell 
you that they came on in the course of five or six days. 
Such a period is that of an " acute " onset; it is the period 
which suggests that the morbid process is inflammatory. 
But you must never be content with general statements. 
Always strive to obtain details, even when they seem 
superfluous. How important the details may be is usefully 
shown in this case : they change entirely the significance 
of the first statement. We learn, first, that three weeks 
before the symptoms came on he had a brief attack very 
much like that with which the paralysis began. He is 



54 SYPHILITIC HEMIPLEGIA. 

fond, as many wise men have been fond, of finding recreation 
in the violin. One day he found, while playing, that he 
could not draw the bow across the strings. It seemed as if it 
were glued to the strings. Then he found the right arm and 
hand were altogether weak. But in an hour or two all 
this had passed away. Three weeks later the same disa- 
bility recurred under the same conditions, and it was 
accompanied by a peculiar feeling of numbness in the 
right arm and the right leg. When he walked he stag- 
gered, and so he continued until he went to bed. Next 
morning he found the arm and leg had become weaker. 
No change in them occurred during the following day, but 
in the next night complete loss of power came on, so that 
when he awoke he could not move either arm or leg. His 
speech was " thick," and, indeed, had been so upon the 
preceding day. Thus, when closely examined, we have a 
series of sudden attacks, the first in the day, after a sudden 
premonition such as had occurred three weeks before, the 
others in the night. The suddenness of onset during 
sleep we have to infer, but in most cases, when symptoms 
of considerable degree come on during sleep, their onset 
belongs to the class which we call sudden. We have fur- 
ther evidence of the truth of this in the fact that the first 
commencement was definitely, absolutely sudden, and 
succeeded a slight brief attack which was likewise sudden. 
So the details of the development of the symptoms show 
that the onset must be placed among those which indicate 
a vascular lesion. Which of the two processes had 
occurred? Cerebral hemorrhage is excluded by the age 
of the patient. It is not, indeed, excluded by the patient's 
age, in the abstract. Many of you may have seen cerebral 
hemorrhage in a person as young as he is. But you have 
seen it as the subject of a pathological, and not a clinical, 
demonstration. Note the difference implied in this dis- 
tinction. Hemorrhage occurs in the young, but it kills 



DISTINCTION BETWEEN EMBOLISM AND THROMBOSIS. 55 

them. It is not survived, and the fact that this patient is 
very obviously living excludes hemorrhage. It is only the 
subject of clinical demonstration at a much later period of 
life, because the hemorrhage that is survived is the result 
of degenerative changes practically confined to the degen- 
erative period of life, and hemorrhage in the young is the 
result of disease of the larger arteries, such as permits their 
distention into an aneurism, the rupture of which is fatal. 

Vascular obstruction it must therefore be with which 
we have to deal in this case. Veins or arteries may be 
obstructed ; but the veins that are obstructed are on the 
surface of the brain, and we have found evidence that the 
lesion here is not at the surface, so we may put venous 
obstruction on one side. It must be arterial obstruction. 
This may be the result of two causes, which, widely differ- 
ing in origin, have the same ultimate effect. They are 
embolism, closure by a plug brought from a distance, and 
thrombosis, closure by a clot formed in situ. Do not for- 
get the distinction. The advice may seem superfluous, but 
it is curious how the idea of embolism dominates the 
minds of practitioners to the exclusion of thrombosis, and 
they call " embolism " whatever is not hemorrhage. But 
the distinction is quite as important as that between hem- 
orrhage and obstruction. 

An embolus must have a source. Almost invariably this 
source is a valve of the heart. To justify a diagnosis of 
embolism you must find a source, — that is, practically, you 
must find valvular disease of the heart, or, if the attack 
occurred some months ago, you must have a history of 
some malady, not long before the onset, known to cause 
endocarditis. Do not forget this also, because endocarditis, 
recently acute, may cause cerebral embolism, and yet may 
pass away so completely that at the end even of six months, 
not only may there be no murmur, but the walls of the 
heart may have so perfectly resumed their normal state 



56 SYPHILITIC HEMIPLEGIA. 

that you cannot perceive any indication that there has been 
any cardiac disease. In this case no cardiac disease can 
be detected, and, further, no malady can be heard of that 
will cause endocarditis. Embolism may therefore be 
excluded, and we are left with thrombosis as the cause of 
the condition, thrombosis producing a focus of necrotic 
softening. 

But we have not yet done with the process of diagnostic 
analysis. Thrombosis has two causes. It is a clotting of the 
blood, and it may be due only to a strong tendency of the 
blood to clot. This, however, is very rare. It occurs in 
the old and gouty; it occurs in the subjects of cancer; it 
occurs in states of profound general weakness, and it occurs 
especially soon after childbirth, when the vessels of the 
uterus have to be closed by clot, and the tendency to 
coagulation may be regarded as physiological, — physiologi- 
cal, but, unhappily, often also pathological, as the disas- 
trous thrombosis in the pulmonary artery shows us too 
often. But here we have no evidence of such diathetic 
states, no history of general weakness, and, since the 
patient is a man, we may safely exclude the puerperal con- 
dition. 

The second cause of thrombosis to which we are thus 
reduced is disease of the artery at the spot, disease which 
induces the formation of the clot. Such disease thickens 
the wall, narrows the lumen of the vessel, often almost to 
the point of closure. It also changes the inner surface, so 
that this acts like a foreign body, and on it a coagulum 
readily forms. The effect is produced in greatest degree 
on the branches that come off where the wall of the main 
artery is diseased. Beyond the narrowed part the vessel is 
wider, but the narrowing permits little blood to flow 
through, and hence the circulation in the wider partis very 
feeble, and where the narrowing ends we have the change 
in the wall. Hence chronic disease of the walls of the 



DIAGNOSIS OF SPECIFIC DISEASE. 57 

arteries leads to sudden occlusion by the formation of a 
clot, and gives rise to symptoms of sudden onset. 

There are only two forms of arterial disease which act 
upon the arteries going to the central ganglia of the brain. 
A third cause, traumatic arteritis, only acts upon the arte- 
ries of the convex surface, and it is, moreover, extremely 
rare. You know, probably, what the two conditions are, 
— atheroma and syphilitic disease. Each has the same 
effect; in each there is a thickening of the wall, a narrow- 
ing of the vessel, and especially a narrowing of the 
branches which the main trunk gives off at the spot, for it 
is generally a main trunk which is the seat of the change. 
But atheroma is a senile lesion. It is a disease of the old, 
even more emphatically than is hemorrhage, for in extreme 
old age it becomes the more common lesion of the two. 
But this disease also the patient's age excludes. 

By the mode of onset and the age of the patient, taken 
together, we thus arrive at the diagnosis that the cause of 
the symptoms must be an area of softening due to syphi- 
litic arterial disease. 

The time occupied by the onset, although the chief, is 
not the only guide. We may leave out of consideration 
those indications which apply only to patients in the later 
period of life, which we shall have another opportunity of 
considering. In the early period the distinction between 
the two common causes of hemiplegia, embolism, and 
thrombosis from syphilitic disease — for these two embrace 
certainly ninety-five per cent, of the cases of sudden onset 
in early adult life — is sometimes aided by the presence or 
absence of symptoms before the onset. Until the moment 
when an embolus is carried with the rushing blood into a 
vessel too small for it to traverse, the state of the intra- 
cranial structures is normal. In embolism, therefore, we 
have no premonitory symptoms. But it is not so in arte- 
rial disease. The narrowing of the arteries and the 
6 



58 SYPHILITIC HEMIPLEGIA. 

morbid process which is going on in their walls might be 
expected to cause symptoms constantly. It does so fre- 
quently, but not constantly, apparently because thrombosis 
occurs earlier, and with less extensive disease, in some 
cases than in others. One patient has headache, another 
has tingling or transient attacks of slight weakness in the 
limbs afterward paralyzed, the result of the interference 
with the blood-supply to the region from which it is after- 
wards altogether cut off. This patient had no premoni- 
tory symptoms in the limbs, but he had headache for a 
month, greater during the week immediately preceding 
the onset. So that this symptom yields us another indica- 
tion pointing to the same conclusion as that to which we 
have been conducted by the study of the onset and the 
process of successive exclusion. 

Loss of consciousness at the onset is chiefly important 
when the distinction has to be made between hemorrhage 
and softening. In the latter it is more often absent than 
present, and it was absent here. The only help it gives 
is that it is rather more often absent in thrombosis than in 
embolism, because the latter is more violently sudden, and 
it seems to give rise to a more definite shock to the brain. 
So this indication also affords confirmation of our opinion ; 
although it is slight it corresponds in direction with the 
rest, a correspondence you should never fail to notice. 

There are other occasional peculiarities of onset which 
afford a distinctly useful indication, and such is the onset 
of the symptoms in the patient before you. When the 
paralysis comes on in a series of distinct sudden attacks, 
each without loss of consciousness, each increasing the 
extent or degree of those which preceded it, we have a 
form of onset which is seldom, very seldom, met with ex- 
cept in thrombosis. The successive attacks mean the 
successive occlusion of branches of the diseased vessel. 
When hemorrhage has a deliberate onset it is gradually 



CONFIRMATORY EVIDENCE SOUGHT. 59 

progressive from the slow forcing of blood into resistant 
tissues, or there are but two stages, of which the second 
is attended with profound coma and general paralysis, be- 
cause it is the expression of rupture into the ventricles of 
the brain. Thus, in this patient the features of the onset, 
and its immediate antecedents, entirely confirm the opinion 
to which we arrived from the comparative study of the 
pathological possibilities. 

Yet there remains another question of ultimate impor- 
tance which may destroy our inference, leave it unchanged, 
or strengthen it. It is the question whether any evidence 
of the assumed cause of the morbid process can be ascer- 
tained. That, in most cases, is the form in which the 
question must be put. But if no cause of any one of the 
possible lesions can be traced, it is necessary to consider 
whether the cause of that which is otherwise indicated can 
or cannot be excluded. If it cannot, the indication may 
be followed. Hence, in the case before us, having found 
that syphilitic disease is the probable cause of the cere- 
bral lesion, we ask, Has the patient had syphilis ? To 
this the answer is an uncompromising negative. We can 
ascertain no history of any primary lesion or of any second- 
ary manifestation of the disorder which we assume to be 
the cause of the morbid process which has brought him 
now under our observation. Some of you, and many of 
those who are not conversant with the progress of recent 
observation, would be inclined to accept the negation as a 
decisive disproof of our conclusion. They would be 
wrong. We have here a pertinent illustration of the im- 
portance of the absence of disproof where proof has been 
found wanting. Those who see many patients suffering 
from syphilitic affections of the nervous system, see 
among them some who, as this patient, can give no ac- 
count of any chancre or of any secondary symptoms, and 
among these there are some in whom a minute and care- 



60 SYPHILITIC HEMIPLEGIA. 

ful examination reveals some conclusive indication of 
syphilitic disease, it may be in the tongue, in the throat, 
on the face, or in the eye, but it shows how small is the 
practical importance of the ignorance which might seem 
to some to be conclusive. There are others in whom no 
such indication can be found, but who at some future time 
come under our notice with distinct later symptoms un- 
mistakably syphilitic. Now, the existence of these two 
facts makes it impossible for us to accept the patient's 
belief that he has never had syphilis as destructive of our 
diagnosis. All that it does is to cause us to ask that 
second question, Can the patient have had syphilis ? The 
disease is, for practical purposes and outside the ranks of 
the medical profession, acquired in only one way. If there 
has been no exposure to the risk of contagion, we may 
exclude the disease and we must be wrong in our diagno- 
sis. If there has been such exposure to possible con- 
tagion we may be right, and a sufficiently extended 
observation compels us to regard the negative history as 
then without significance. It is so in this case. For five 
or six years the patient has been frequently exposed to 
the risk of contagion, and therefore we may regard our 
diagnosis as unaffected by the negation, and regard it as 
the expression of ignorance of the malady, not necessarily 
of its non-existence. 

One or two features in the symptoms and in the lesion 
should not be passed by. The general symptoms of hemi- 
plegia, as I said, we will defer, but almost every case pre- 
sents some special features which we may not soon meet 
with again. Notice that the hand, although weak, presents 
no complete paralysis of any movement, but notice also 
that the movements are a little irregular. When he tries 
to touch his nose with his first finger, and eyes shut, he 
does not carry the tip of the finger straight to the tip of the 
nose. Such defective co-ordination is common with mod- 



DIAGNOSTIC SYMPTOMS. 61 

erate recovery of power, and has not, as far as we at present 
know, any definite significance. It is not here associated 
with the symptom which some patients present, an ignor- 
ance of the position of the hand on passive movement. 
Next observe that sensation is unimpaired throughout the 
side. From this we infer that the posterior third of the 
hinder limb of the internal capsule has escaped, and there- 
fore that the adjacent grey matter has escaped ; and we 
are, therefore, prepared for another negative fact which you 
should always ascertain and note, that there is no hemiano- 
pia. There is no affection of sight, and there are no mor- 
bid changes in the eye. Syphilitic disease of the arteries 
and its results never cause optic neuritis. If there is optic 
neuritis you may feel sure that, in addition to the arterial 
disease, there is a syphilitic growth in some position in 
which it has not caused symptoms. 

Lastly, look at the movements of the face, and remem- 
ber that in all cases of facial paralysis it is necessary to ob- 
serve the amount of interference with three different kinds 
of movement which take place in the face, especially in the 
lower part, which alone is involved in this case. The first 
is voluntary movement. When told to raise his upper lip 
and put his teeth together, you see that the movement is 
considerably less on the right side than on the left. The 
second is emotional movement, which is best manifested in 
the smile. But it does not do to tell the patient to smile. 
A patient who smiles to order produces only a voluntary 
and not a true emotional movement. To observe the latter 
you must produce the emotion. You may tickle a child, 
but you cannot well, without loss of dignity, adopt this 
method in the case of a grown-up person. But you may 
generally obtain what you need by asking the patient, as I 
now ask this patient, to " favor us with a graceful smile." 
You see that there is much less difference between the 
movement of the two sides than in the voluntary move- 



62 SYPHILITIC HEMIPLEGIA. 

ment. Remember that this difference exists only when the 
disease is in the cerebral hemisphere, or at least above the 
middle of the pons. It is not seen in any case in which 
there is disease of the facial nerve, or its root fibres, or its 
nucleus. Lastly, the associated movement of the face, 
which occurs when the patient exerts force with some other 
part of the body, when he grasps with energy, for instance, 
may present a difference from the voluntary movement 
similar to that which is observed in the case of the smile. 
It may be far more equal on the two sides, and often no 
difference can be detected. We do not yet know the signifi- 
cance of these differences when there is disease in the 
hemisphere, but they show that the cause of the facial 
weakness is in this position, and they will probably ulti- 
mately prove to have a special meaning. The last point is 
the state of reflex action. The patient presents an in- 
creased knee-jerk and a foot-clonus on the right side ; 
these, as you know, show that there is secondary degener- 
ation in the pyramidal fibres. But the plantar reflex is 
almost absent on the right side while active on the left, and 
there is a distinct difference in the abdominal reflex, al- 
though it is less conspicuous, because, as is often the case 
in adults, this reflex action is not readily obtained. Such 
a contrast between the two forms of reflex action is com- 
mon in hemiplegia, and is very remarkable. It is also 
mysterious, because we do not yet know to what the dimi- 
nution of reflex action from the skin is due. It is present 
immediately after the occurrence of the cerebral lesion, 
while permanent increase in the myotatic irritability does 
not manifest itself until toward the end of the first week. 
We urgently need a series of careful observations on the 
position of the cerebral lesions in cases in which this dimi- 
nution in the superficial action is present, and their posi- 
tion in the cases in which it is unchanged. It is not a 
recondite subject, and I would commend it to your notice. 



ILLUSTRATION OF DISEASED ARTERIES. 63 

Regarding the lesion, several points demand our notice. 
What is the change in the walls of the vessels which we 
have assumed to exist in this case ? I show you under 
the microscope some sections of such diseased arteries, 
which have been prepared by Dr. Taylor. They show very 
beautifully the main features of the morbid change. You 
can see that there is a very extensive growth of cells and 
fibres in both the inner and outer coat of the vessel, the 
separation between the two being indicated by the wavy 
line of the elastic lamina. You may also see that the 
growth has almost closed the chief vessel, and that some 
branches which are divided in the section are completely 
occluded. 

This disease of the arteries causes nodular swellings on 
the external surface, often considerable in their promi- 
nence. They are less translucent than the normal wall, 
but less opaque than the enlargement which occurs in 
atheroma. That is because, prone as syphilitic tumors are 
to undergo caseation, the tendency is slight in these arte- 
rial growths, and hence we have not the dense opacity 
which is due to fatty degeneration in the senile lesion. 
The change is especially common on the basilar artery and 
on the middle cerebrals, and in this case we can have little 
doubt that such disease in the left middle cerebral has oc- 
cluded those branches which go to the central ganglia 
through the anterior perforated spot. It probably has not 
arrested the circulation through the main trunk, and so 
the cortex is intact and the patient has escaped the impair- 
ment of speech, which is the common result of the soften- 
ing of the cortex, which occurs when the main trunk of 
this vessel is occluded. 

But I would call your attention to one point, which is 
not, I think, remarked in any text-book. If the patient 
has been subjected to treatment, the disease in the wall of 
the artery is considerably changed. The swelling dimin- 



64 SYPHILITIC HEMIPLEGIA. 

ishes and may be scarcely recognizable, but the wall is still 
a little thicker and a little more opaque than normal. The 
aspect resembles that of slight atheroma far more closely 
than does the syphilitic disease in its recent and unaltered 
state. You must therefore be prepared for this appearance 
in the case of many patients who have been under the care 
of those who recognized the cause of the symptoms. Often 
you find such old disease, altered in the manner I have 
described, in one artery, and in another artery recent 
change of characteristic aspect. Not long since I met with 
a very instructive example of this, most instructive, also, in 
its clinical manifestations. The patient was a doctor, thirty- 
five years of age, of reticent habits, who had suffered from 
a sudden brief attack of loss of speech. Six months before, 
he was attacked with sudden symptoms of an extremely 
grave character. Rising in the morning well, although 
there was some reason to believe that he had suffered from 
headache for a few weeks, he was suddenly attacked with 
difficulty of articulation and with mental stupor, deepening 
in a tew hours almost to coma, and attended by paralysis 
of the right arm, right leg, and lower part of the face, com- 
plete paralysis of the muscles of the left eyeball, and almost 
complete of those of the right, with immobility of the 
pupils, the right being small and the left dilated. So he 
continued for two or three days, and then, with rising tem- 
perature, he died. The symptoms pointed conclusively to 
a lesion of the oculo-motor nuclei beneath the corpora 
quadrigemina, greater on the left side and extending 
through to the motor tract, a lesion of sudden onset, and 
therefore vascular, and, from the reasons we have consid- 
ered in our review of the case before us, certainly due to 
vascular occlusion, to arterial disease, and almost certainly 
to syphilitic disease of the basilar artery and posterior cere- 
brals. The attack six months before might reasonably be 
ascribed to similar disease in the middle cerebral of the 



POST-MORTEM CONFIRMATION. 65 

left side, disease which, on the assumption that he was 
conscious of previous syphilis, would naturally lead him to 
take iodide of potassium, the influence of which would be 
to prevent, for the time, further effects of the disease. He 
could easily have obtained it, and would have been un- 
likely to communicate his apprehensions or self-treatment 
to any person. The omission of the drug, or possibly, 
even, as we shall presently see, its too long continuance, 
would have permitted a fresh development of arterial dis- 
ease in the basilar and posterior cerebrals, with resulting 
and fatal thrombosis within them. Such was the opinion 
expressed on the first examination of the patient, the day 
after the onset, and the subsequent condition affoided me 
no grounds for changing the diagnosis. The post-mortem 
examination showed its correctness in a degree which 
would be remarkable, were it not that the elements of the 
diagnosis were simple, and only required trust in the pro- 
cess of reasoning to induce confidence in the conclusion. 
There was thrombosis of the front of the basilar, extending 
into the posterior cerebrals, further into the left, and on 
this there was a characteristic nodule of syphilitic disease, 
while slighter thickening, narrowing the cavity of the ves- 
sels, was seen on the other posterior cerebral and on the 
front of the basilar. In the middle cerebral, within the 
fissure of Sylvius, was an area of altered wall of greater 
opacity and thickness, but without much prominence, pre- 
cisely the aspect I have mentioned to you as left by syphi- 
litic disease which has been removed by treatment, and 
justifying the opinion that I have mentioned. 

What is the relation of the vascular lesion to the consti- 
tutional affection ? Although not yet demonstrated, it is 
impossible to doubt that syphilis, like every disease that is 
transmitted by inoculation, that has a period of incubation 
and is first manifested by exanthematous and allied symp- 
toms, depends on a specific organism which multiplies in 



66 SYPHILITIC HEMIPLEGIA. 

the system and produces germs. As far as we can read 
the meaning of the course of this malady, it would seem 
that the various morbid processes which it causes are the 
result of the presence of developed organisms, abundant 
in the blood in the exanthematous stage, and leaving germs 
which rest in some tissue until a time comes when they 
develop and give rise to a process of tissue-growth such as 
that which we have been considering in the walls of the 
arteries. 

Accumulated and accumulating experience leads us to 
the conclusion that the remedies employed for this disease 
— mercury in the first rank and iodide of potassium in the 
second — destroy the developed and developing organisms, 
and remove, or promote the removal, of the tissue-growth 
which the organisms have caused. Hence the manifesta- 
tions of the disease in the early florid stage, or the later 
occasional effects, may be with certainty swept away. But 
the agents seem to have no influence on the germs which 
are deposited in the system and are not yet in the process 
of development. You are doubtless familiar with the fact 
that the germs of bacterial organisms have far greater 
power of resistance than the organisms themselves ; that 
they resist, for instance, temperatures which are fatal to 
the latter. Hence the removal of the symptoms at any 
stage of the disorder does not free the patient from the 
liability to the occurrence of future symptoms, the result 
of the development of the germs that have been untouched 
by the therapeutical agent that has been employed. The 
most thorough treatment at any stage of the disease does 
not prevent its future manifestations, and the freedom from 
these is as frequent in those who are not so treated as in 
those who are. It depends on the disease, on the amount 
of organized material in the system, and on no other ele- 
ment. It is in this sense that I have expressed my con- 
viction that syphilis as a disease is not curable. I have 



UNFAVORABLE PROGNOSIS. 67 

been taken' severely to task for the assertion, but it has 
received no dissent from those who know most of the 
malady, and whose opinions deserve chief attention. I 
believe that the statement is the assertion of an incontro- 
vertible truth. 

All that we have hitherto considered is but the path to 
the problems that are of practical moment, — those that 
concern the interest of the patient, — and, therefore, to us as 
practitioners are of paramount importance. These are the 
prognosis and the treatment, the attempt to forecast the 
future, and the attempt to remove or lessen the symptoms 
and to prevent their return. 

Strive, gentlemen, when you consider the prognosis of 
such affections, to form a mental picture of the morbid 
process. Note its elements, their mutual relation, and their 
relation to the symptoms. You may perhaps be surprised 
to perceive, when you do this, that in all cases of true 
syphilitic lesions of the nerve-centres the symptoms do not 
directly depend, in every case, upon the syphilitic process 
itself. This is conspicuous in the case of the disease with 
which we have to deal to-day. The symptoms depend on 
the necrotic softening of the brain, which is precisely the 
same as that which would be caused by any other form of 
arterial closure, by embolism, or by thrombosis due to any 
other mechanism. It is the result of the arrest of the 
blood-supply, and the clot which finally stops this is also 
common and not specific. It is only when we reach the 
cause of the narrowing of the artery that we reach the 
actual syphilitic element in the process. But you cannot 
fail to perceive, further, from these facts, that the course 
of the symptoms must be altogether independent of the 
course of the arterial disease which led to the obstruction. 
Remove the disease in the artery ; it still remains imper- 
vious, and ultimately becomes a mere fibrous thread ; 
nothing can restore its cavity and the destroyed brain-tissue 



68 SYPHILITIC HEMIPLEGIA. 

also nothing can renew. Such a patient will improve, 
partly by the recovery of the least damaged structures, 
partly and chiefly by the compensation which happily the 
other hemisphere is able to effect in the case of all move- 
ments which are related to both sides of the brain, those in 
the upper part of the arm and face, and the chief move- 
ments of the leg. But the future course of the paralysis, 
in every case of the kind, will be the same as if the 
obstruction were the result of embolism, and the fact must 
be frankly recognized. Do not, as is so often done, assure 
a patient with hemiplegia of a year's duration that he will 
recover, because his malady was the result of a process 
which you know can be removed, and which most likely 
has already been removed. 

Is treatment therefore useless ? By no means. Its 
importance is great, and the greater the sooner after the 
onset you can apply it, and it is greatest of all before the 
onset, when the shadow of the coming disaster is thrown 
by premonitory symptoms, and when the substance may 
very often be averted by the prompt recognition and 
energetic treatment of the morbid process. I am certain 
that in cases which have come under my notice this result 
has been achieved, and palsy, perhaps life-long, and some- 
times even death, have been averted. In this patient we 
have an illustration of the opportunity which many others 
present: when he first felt the disability in the arm, the 
merest suspicion of its possible cause would have justified 
treatment which would certainly have averted the sequel. 
After the closure has done its work, and the softening has 
produced its symptoms, treatment can do nothing for that 
which is, but it may still do much for that which may be. 
We cannot tell how many other arteries are diseased, how 
many other branches are in imminent danger of being 
closed, and it is essential, therefore, at once to give the 
patient iodide of potassium, seven or ten grains three times 



TREATMENT. 69 

a day, and even fifteen grains for the first few days, with, 
if you like, mercurial inunctions. I believe that this dose 
of iodide is adequate, and will do all that can be done in 
the course of four or six weeks. It is better not to give 
larger doses, because coagulation of the blood plays a part 
in the mechanism of destruction, and large doses of iodide, 
as the treatment of aneurism has taught us, increase the 
tendency of the blood to clot. Of even more importance 
is it not to continue the iodide beyond six weeks or, at 
most, two months. In that time, as visible processes show 
us, all the specific element in the process is removed. If 
recovery is not complete, it is because the simple elements 
may take yet a longer time to pass away, or may be of 
such deeper character that they must persist. If you go 
on with iodide for four or six months, you may find the 
process that was at first arrested regains activity, and the 
very same syphilitic process may actually kill the patient, 
in spite of the continuance of the treatment which at first 
arrested it. Apparently the organisms become acclimatized 
to the presence of the agent, are able to resist it, and thrive 
in spite of it. Analogous phenomena are known, as I 
have hinted in the case of similar organisms and the effect 
of high temperatures. But while you should not continue 
the treatment, you should always resume it. After three 
or four months' cessation it is as effective as at first. 

I consider that every patient who has had syphilis should 
for at least eight years from the primary disease, or five 
from the last manifestation of it, take a course of iodide for 
three weeks twice a year. In this way developing organ- 
isms which have not yet caused tissue-changes sufficient 
to produce symptoms may be destroyed, and in many cases 
it is certain that this measure would save the patient from 
grave disease. We cannot see the result, but in this it is 
but on the level of all the other forms of preventive medi- 



70 SYPHILITIC HEMIPLEGIA. 

cine, the branch of our professional work to which we may 
look up with the highest pride, and go on with, confident 
in its unseen achievements, despite the fact that the recipi- 
ents of its greatest blessings are all-unconscious of them, 
as they are always of the health they enjoy until they lose 
it, and of the air they breathe until the last breath may 
bring- to their mind the flash of revelation, all too late. 



LECTURE V. 
BULBAR PARALYSIS. 

Gentlemen : — I wish to-day to take the opportunity that 
this case affords me of showing you the symptoms of the 
malady generally known as " bulbar paralysis." It was 
formerly called by a descriptive designation, given to it by 
Duchenne, " labio-glosso-laryngeal paralysis." The symp- 
toms in this case are so complete in degree that they may 
impress upon your memory the chief features of this 
malady. You are not likely to forget them after you have 
observed a well-marked case. 

Let us first briefly note what they are. (i) You will 
observe, when I tell the patient to move his lips and mouth, 
that he has but little power of moving the lower part of 
the face; although he can put in perfect action the muscles 
of the forehead and eyelids. He can only slightly raise 
the upper lip ; he cannot narrow the orifice of the mouth ; 
although he can just approximate the lips, it is imperfectly; 
a slight chink remains between them, and they cannot be 
kept together. (2) His tongue is almost completely para- 
lysed ; when he tries to put it out, you see that he cannot 
get the tip beyond his teeth. Moreover, if you look at 
the surface of the tongue as it lies in his mouth, you will 
see that it is uneven ; irregular depressions upon it indi- 
cate the atrophy of the muscular tissue of which it chiefly 
consists. (3) His palate can be raised, but if he tries to 
swallow, liquids come back through his nose, evidence 
that the palate does not shut off, as it should, the cavity of 

Clinical Journal, May 2, 1894. 
71 



72 BULBAR PARALYSIS. 

the nose, on account of feebleness of the palatine muscles. 
But semi-solid food is swallowed well ; it does not regur- 
gitate into the nose, and when it has once reached the pha- 
rynx it is passed down into the oesophagus without diffi- 
culty. This is proof that the pharyngeal muscles are not 
paralyzed. (4) It is very different with the muscles of the 
larynx. When he tries to phonate he only succeeds in 
making one uniform vowel sound, not altered by any 
changes of intonation. When he tries to cough, you can 
readily perceive, by the sound, that he does not close his 
glottis ; there is a rush of air through the larynx, but there 
is no true cough, for which, you know, the glottis needs to 
be first closed and then suddenly opened. The paralysis 
which is thus indicated can be seen by the laryngoscope. 
Dr. Semon has been good enough to examine his larynx, 
and finds that the left vocal cord is near the middle line, 
and cannot be moved away from it, but the right is habit- 
ually some distance from the middle line, so as to leave a 
space of about 4 mm. between the two. When he tries to 
bring the cords together, the right moves toward the left, 
but does not reach it. In the movement, both cords pre- 
sent a peculiar tremor. The left cord thus presents abduc- 
tor paralysis, while in the right adduction is most affected. 
It is fortunate for him that there is not loss of abduction 
on both sides. If there were, he could probably cough 
and utter vocal sounds much better, but his life would be 
in constant danger, because, as you doubtless know, when 
the cords cannot be separated, the slightest catarrhal swell- 
ing suffices to close up the narrow space that remains, 
and, unless an opening is made into the larynx below the 
glottis, breathing becomes impossible, and the inevitable 
result ensues. 

So this man presents paralysis of his larynx, palate, 
tongue, and lips, together with the lower part of the face. 
The malady has come on gradually, in the course of the 



RELATION OF SYMPTOMS TO FUNCTION. 73 

last two years, and the first part to suffer was that which is 
now most affected, the larynx. He first found that he 
could not sing ; then that he could not speak well, from 
weakening of the tongue ; gradually the other symptoms 
were added. Thus, it is an example of slow gradual bulbar 
paralysis, a malady which we know depends upon a slow 
degeneration of the structures of the medulla oblongata 
concerned in the movements for articulation. Let us glance 
briefly at the parts that are affected. In doing so I would 
ask you to notice how remarkably the affection corresponds 
to their functional use. Those are paralysed which are con- 
cerned in articulate speech. Some of these are also con- 
cerned in deglutition, and hence swallowing is to some 
extent affected, but the fact that the pharnyx is not para- 
lysed is proof of the manner in which the functional limita- 
tion of the affection has spared the special act of swallow- 
ing. We shall presently see the reason for paying such 
close attention to the relation of the symptoms to function. 
It is a point of great importance because it is of great signifi- 
cance, and you should always ascertain how far it is to be 
traced. It is one of the chief features to be attended to in 
each case that comes under your notice. 

This bulbar paralysis is generally a disease of the nuclei 
of the nerves which convey motor power to the muscles 
affected, and when such, it is a disease of the medulla 
oblongata analogous to the degeneration of the motor 
nerve cells of the spinal cord which gives rise to the symp- 
toms of "progressive muscular atrophy." In the medulla, 
you will remember, the regular arrangement of nerve cells, 
root-fibres, and nerve-roots, which obtains in the spin il 
cord, gives place to a very irregular arrangement, in which 
the fibres which subserve a certain function are, for the 
most part, gathered together in a single nerve, and rise 
from a defined group of cells, the nucleus of the nerve. 
The irregularity is indeed far greater in the case of the 
7 



74 BULBAR PARALYSIS. 

sensory than in that of the motor fibres, for almost all 
the sensory fibres leave the medulla as a single nerve, the 
fifth, which represents the posterior roots of all the motor 
cranial nerves. But the irregularity is chiefly in the way 
it leaves the brain, for within the pons the fibres of the 
nerve at once separate ; some ascend and some descend, 
and all seem to end in sensory nerve cells at about the 
level of the motor cells to which they are related, as do the 
sensory fibres of the spinal nerves. But the malady we 
are now considering is one of motion, not of sensation, and 
so we may dismiss the sensory fibres of the fifth nerve from 
further consideration, and attend only to the arrangement 
of the motor nerves and nuclei, whose function is so con- 
spicuously impaired. 

As we pass up the cervical region of the cord, before we 
reach the medulla, we have, as it were, an intimation of 
the coming irregularity. The nerve-fibres for the muscles 
of the neck in part arise, and leave the cord, as do the 
motor fibres lower down. But some of them, arising from 
the same anterior grey matter, pass outwards instead of 
forwards, and leave the side of the cord, instead of the front, 
to form by their junction a nerve which ascends to the 
medulla and passes within the foramen magnum as if it 
were trying to attain the dignity of a cranial nerve. It 
does actually join one of the bulbar nerves for a short dis- 
tance, and so this is called the " spinal accessory," but its 
fibres have to separate from the bulbar nerve, and descend 
to the neck, where, as you will remember, it supplies the 
sternomastoid and the trapezius, muscles that serve to 
rotate the head. I mention this nerve thus specially, 
because the bulbar nerve, which its fibres join for a short 
distance, particularly concerns us. The grey matter from 
which it comes would be continuous with that from the 
neck muscles, had not its relation to the other parts been 
deranged by the fibres of the anterior pyramids of the 



DERANGEMENT OF MOTOR NERVES. 75 

medulla, which here cross the middle line and cut up the 
anterior cornua. The cells for the spinal accessory in the 
medulla are the lowest of the bulbar groups. Just as the 
spinal part of this nerve goes to the external muscles of 
the neck, the bulbar part goes chiefly to the internal mus- 
cles of the neck, the muscles of the larynx. But you per- 
ceive that there is a great difference between the two parts 
in source, in destination, and in function, and this difference 
is reproduced in disease. In the patient before you the 
outer spinal part of the nerve is not paralysed ; the inner, 
bulbar part, as we have seen, is almost completely para- 
lysed ; the cells of its nucleus must be extensively diseased. 
If we pass upwards still higher, in observing the parts 
affected, we come to the palate ; this is supplied by the 
same nerve, the spinal accessory, but probably by fibres 
that arise from its highest cells. The supply of the palate 
by this nerve has only lately been proved, but it has been 
proved beyond the possibility of doubt, and the fact is of 
much interest in connection with such a case as this. 

Next, after the affection of the palate, we pass to that of 
the tongue, which is so severe. The hypoglossal nucleus 
lies parallel to that of the inner part of the spinal accessory, 
at first below it, afterwards to the inner side of it. Not 
only are the nerve cells for these three parts near together, 
but so also are their nerve fibres, as they leave the medulla, 
and the tongue, palate, and vocal cord are often paralysed 
together by a morbid process at the surface, damaging the 
nerve roots. 

How closely structural relations reproduce those of func- 
tion, how, indeed, they determine the latter, is again illus- 
trated by the last part of the combined paralysis which we 
have to consider, that of the lower part of the face, and es- 
pecially the lips. The chief nucleus of the facial nerve is 
only a little above the upper extremity of the hypoglossal. 
The nerve leaves the pons above the level of its chief nu- 



76 BULBAR PARALYSIS. 

cleus, to which its fibres pass downwards by a somewhat 
circuitous course. But the relations of the fibres of the 
nerve which subserve its particular functional relations are 
still, in the main, unknown to us. The muscles supplied by 
it have a twofold function (i) in connection with articula- 
tion, in which the lower functional muscles are chiefly con- 
cerned, and, in particular, those of the lips. These are the 
muscles which are so much affected in the case before you. 
(2) The muscle which closes the eyelids is concerned, in its 
function, with the muscles of the eyes, and this is also true 
to some extent of the muscles of the forehead, for when we 
look up the frontales raise the eyebrows, and when the eye 
has to be protected by a strong contraction of the orbicu- 
laries, the corrugator assists. (3) All the muscles of the 
face are concerned in the expression of emotion, the upper 
as well as the lower muscles of the face. It is only the first 
of these three functional relations which concerns us now. 
It is certain that there must be a close connection be- 
tween the fibres or cells which have to do with the muscles 
about the mouth, and with those for the tongue, but the 
anatomical connection has not yet been traced. That there 
is such an anatomical connection, we cannot doubt, nor can 
we doubt that it is especially diseased in such a case as this. 
Apart from the evidence of the relation afforded by disease, 
I may call your attention to a curious proof that is to be 
obtained, even under normal conditions, of the closeness of 
the relation between the tongue and the lips, and also be- 
tween the fibres or cells of the facial and hypoglossal nerves 
which innervate the parts. Try to narrow your tongue ; 
you will find you cannot do so without, at the same time, 
narrowing the opening of the mouth. You cannot contract 
the transverse fibres of the tongue without also contracting 
the transverse fibres which run in the lips. If you try to 
do either of these you will find that you do the other also. 
The experiment succeeds best, or at any rate we are most 



CORRESPONDENCE OF PARALYSIS TO FUNCTION. 77 

conscious of it, if the tip of the tongue is first placed be- 
tween the lips. Try it now, and your sensations will speed- 
ily convince you of the truth of the statement. 

Thus the symptoms are dependent on a paralysis of the 
muscles supplied by part of the facial, part of the spinal 
accessory, and by the hypoglossal nerves. 

The paralysis corresponds to function in its distribution, 
and has been gradual in development. These two features 
are always evidence of the degenerative nature of the process 
on which the paralysis depends. 

But it is important to note that there are two forms of 
this chronic bulbar paralysis. I have told you that these 
nerves and their nuclei, although situated in the medulla, 
correspond to the motor nerves and motor grey matter of 
the spinal cord. The same correspondence is to be traced 
in the chronic palsies which affect the two parts. In the 
limbs we may have the same two forms of paralysis. We 
may have the slow paralysis confined to the wasting muscles 
and dependent on the degeneration of the grey matter of 
the spinal cord from which the motor fibres proceed. We 
may also have a slow paralysis without wasting, but with 
excess of the muscle-reflex action, and this, as you prob- 
ably know, depends on a slow degeneration of the fibres 
which conduct the voluntary impulse from the brain to the 
spinal grey matter. In some cases of chronic bulbar par- 
alysis we have conspicuous wasting of the parts paralysed, 
and then we always find degeneration of the cells of the 
nuclei from which the fibres proceed, especially conspicuous 
in the cells of the hypoglossal nuclei. This form is often 
associated with the corresponding muscular atrophy in the 
parts supplied by the spinal nerves, especially in the arms. 
In such a case, however, we have no wasting, but a slow 
paralysis similar to that which I have described as met with 
in the limbs. Although the precise lesion in this case has 
not yet been made out there can be little doubt that it de- 



78 BULBAR PARALYSIS. 

pends on a degeneration of the fibres which convey the 
voluntary impressions from the brain to the nuclei. These 
pass with the fibres for the limbs until a short distance 
above the nuclei, and then they pass across the middle line 
to reach the nerve cells for which they are destined. The 
fibres for the limbs cross the middle line chiefly at the 
"decussation of the pyramids." 

The only explanation of such cases that we can give is 
that, in them, these upper fibres suffer just as do those in 
the spinal cord in primary lateral sclerosis. In the spinal 
cord the degeneration probably begins at the lower ex- 
tremity of the fibres and extends upward, precisely as it 
does in the peripheral nerves in some forms of multiple 
neuritis, and we may reasonably assume that the affection 
of the similar fibres for the nerve-nuclei of the medulla has 
a corresponding course. If so, we are able to understand 
the strict correspondence with function which may be often 
discerned in such cases, as well as in those in which the 
nuclei themselves suffer and the muscles waste. Even in 
the case of the degeneration of the peripheral nerves, the 
correspondence with function is often remarkably close. 
But in both forms of bulbar paralysis the degree of corre- 
spondence with function varies. In the patient before you 
it is strict; in the case from which I am about to show you 
a section, not only the muscles in articulation, but also 
those in deglutition, were affected ; the pharynx was para- 
lysed as well as the larynx. We are not able, at present, 
to attach any special significance to this difference ; it is 
possible that some day we may find in it an important indi- 
cation of the cause of the disease. 

These then are the two forms of chronic bulbar paralysis. 
Because the nuclei that are affected are those for the lower 
cranial nerves, it is sometimes called " inferior nuclear 
paralysis;" the group of nuclei in the upper part of the 
mid-brain, those which innervate the eye muscles, are some- 



VARIOUS FORMS OF THE DISEASE. 79 

times affected in a similar manner in what is called " supe- 
rior nuclear paralysis." It is indeed "superior" only as 
regards the chief nucleus affected ; in this we have an inter- 
esting instance of the way in which function, rather than 
locality, determines the grouping of degeneration. The 
nucleus of the sixth nerve, you will remember, is quite low 
in the pons ; so low, indeed, that the facial nerve, which is 
affected in the inferior palsy, actually winds round it, and 
yet this nucleus is involved with that of the third nerve in 
the superior nuclear palsy giving rise to the affection which 
has also been termed " ophthalmoplegia externa." In other 
rare cases both sets of nuclei suffer, generally, however, in- 
completely. Some of you may remember a woman who 
has attended here, who has a considerable degree of superior 
nuclear paralysis and a slight degree of inferior paralysis. 
I shall have to allude to her case again, because it is remark- 
able in being a sequel to diphtheria. 

The two forms of chronic disease which I have described 
do not include all the cases of bulbar paralysis. There is 
also an acute form, or rather, I should say, a sudden form, 
which depends upon the closure of some of the arteries 
which supply this part with blood. The closure is the 
result of disease of the main trunk from which the small 
arteries spring ; thickening of the wall necessarily entails 
the narrowing of the orifice of the branches that arise there. 
Most of the blood comes from branches which pass near 
the middle line, either from the vertebral or from the basilar 
artery. The resulting paralysis is generally much more 
irregular than in the degenerative chronic variety, as we 
might expect it to be, since the effect of vascular disease is 
always to cause a more or. less random lesion. When one 
vertebral is diseased, and the branch which is closed comes 
from it, the affection is chiefly one-sided. Now and then, 
however, even when thus produced, it is bilateral, and the 
explanation of this, at first puzzling, fact is to be found in 



80 BULBAR PARALYSIS. 

the frequent disparity in size of the two vertebrals. This 
disparity may be such that the nerve nuclei near the middle 
line, which are those especially diseased, are supplied with 
blood on both sides by the branches which come from the 
one large vertebral artery. Then, of necessity, disease of 
that artery and closure of the branch cause symptoms 
which are bilateral and symmetrical. I will show you in a 
moment an example of this instance of bulbar paralysis. 

There is yet a fourth variety to be considered, which is, 
however, so rare that it may be dismissed with a mere men- 
tion. Very, very rarely these nuclei seem to be the seat 
of a true inflammation, and we then have a bulbar paralysis 
which is not sudden but acute in onset, as the effects of all 
inflammations are. Such a lesion is extremely rare, but it 
is a little less so in the case of the superior group of nuclei. 
It is important, however, to mention it, because it has been 
known to supervene on a chronic degeneration, and to be 
an immediate cause of grave danger. Indeed, if the list is 
to be made complete it is necessary to mention that myste- 
rious cases have been met with in which the characteristic 
symptoms of bulbar paralysis have existed and have caused 
death, although no morbid state could be discovered either 
in the medulla or in the nerves. We can only explain such 
a fact by supposing that there are grave alterations in the 
nutrition of the nerve elements, sufficient to abolish their 
function, which are at present not within the range of our 
means of observation. We know that this is the case in 
chorea and also in paralysis agitans ; although in these 
affections the changes do not abolish function, it is quite 
conceivable that, in the almost inconceivable complexity 
of the molecular nutrition of the nerve cells, alterations 
may occur which do arrest function, and which yet entirely 
elude our present means of detecting them. But it is also 
possible that in some of these cases there may be a degen- 
eration of the fibres which conduct the motor impulse from 



A LAW OF PATHOLOGICAL SIGNIFICANCE. 81 

the brain to the nuclei, and are, in a sense, homologous with 
the fibres that pass to the grey matter of the spinal cord in 
the pyramidal tracts. We have reason to believe that, in 
the latter, the process of degeneration only begins at their 
lower extremities, as it does at the lower extremities of the 
peripheral nerves in most forms of multiple neuritis. In 
such cases degeneration, chronic or acute, may give rise to 
symptoms of considerable severity, although confined to 
the terminations of the fibres, and thus the lesion may 
escape detection. 

Let us now consider in greater detail the facts of the 
malady which is before us, the chronic degenerative bulbar 
paralysis. We know very little of its cause. It is most 
frequent in the old, but it occasionally attacks the middle- 
aged, as in this instance, and now and then, for some reason 
or other, it occurs in those who are still children. .Some 
day we may know the reason of this. At present all we 
can do is to recognise what may be termed the outlines of 
the general causation of such affections. These diseases 
are degenerative. A short time ago this statement would 
have taught us nothing. But we have reason, of late, to 
recognise in most degenerations the evidence of the pre- 
vious action of a toxic influence. Note this important law, 
that the affection of the nerve elements related to function, 
when acute, indicates the action of a toxic influence ; when 
chronic, a degenerative process. It is a law of important 
practical application, but it has also an important pathologi- 
cal significance. The two things are not entirely separated. 
The toxic influence which has no action on the nerve ele- 
ments may yet leave behind it some effect, possibly some 
chemical product, which fixes itself on the nerve elements, 
in consequence of which these nerve elements, at some 
future time, undergo degeneration. This has not been 
proved to be true in the case of bulbar paralysis, but it is 
very probable that it will be proved, at any rate in the case 
8 



82 BULBAR PARALYSIS. 

of the forms which occur comparatively early in life, and 
cannot be attributed to merely senile changes. 

We see this connection between an early toxic blood 
state, and a late degenerative process, conspicuously in the 
case of syphilis and tabes. The same relation is to be 
traced in the case of the superior nuclear paralysis, the 
degeneration of the nuclei for the motor nerves for the 
eyeball of which I spoke just now. This may be asso- 
ciated with tabes, and it may also occur as a late sequel 
of syphilis apart from tabes, a fact of considerable signifi- 
cance. But we cannot trace its relation in the case of the 
inferior nuclear palsy, bulbar paralysis, which especially 
occupies our attention to-day. But some of you may have 
seen a patient who attends here occasionally, and who suf- 
fers from the double affection, from considerable paralysis 
of the ocular muscles, and from slight bulbar paralysis, in 
whom these symptoms have slowly developed as sequel to 
diphtheria. 

We must, however, separate the rare cases that are met 
with before or soon after the completion of development. 
Allied facts suggest* that the cause of these is different. 
They may be analogous to the mysterious " hereditary 
ataxy," " Friedreich's disease," and depend on some con- 
genital defect of vital endurance in the structures concerned. 
But to pursue this would take us too far to-day. The pos- 
sible relation to toxic influences is a subject of great 
importance, because at present we have little power of 
checking the developed disease, but if we can discover such 
a cause, the discovery may bring with it some means of 
prevention or arrest, of which at present we have no indi- 
cation. One other fact deserves mention as bearing upon 
this matter, and that is, that I have once known charac- 
teristic bulbar paralysis to follow ordinary lead poisoning. 
The patient was in the late period of life, and so may have 
been disposed by mere senility to a degenerative process, 



GENERAL LAWS FOR DIAGNOSIS. 83 

but this chemical poison is known to be capable of giving 
rise to a similar process in the motor grey matter of the 
spinal cord, and it must be regarded as a very probable 
cause of the bulbar paralysis in the case in which the 
sequence was observed. 

The general diagnosis of bulbar paralysis resolves itself 
into certain problems, or rather certain general laws. 
First, it is practically only the sudden forms in which a 
distinction has to be discerned from " pseudo-bulbar 
paralysis" — a condition which I have not been able to 
describe to-day. It is the effect of a lesion in each cere- 
bral hemisphere, so situated that the second prevents the 
compensation for the first which is commonly effected. 
The only chronic process which may simulate the bulbar 
degeneration is the slow compression of the medulla, or 
its slow damage by growths inside or outside of it, and the 
symptoms then produced are always irregular, and com- 
bined with other, generally more obtrusive, disturbances, 
which sufficiently indicate the actual nature of the case. 
But the diagnostic difficulties presented by the sudden 
form are numerous. The double cerebral lesion generally 
declares itself by the closeness of two pronounced attacks 
of hemiplegia, first on one side and then on the other, the 
first of which has the common features of cerebral hemi- 
plegia in the affection of the tongue and face on the same 
side as the limbs. It is not uncommon for sudden bulbar 
paralysis to come on in two or three stages by the suc- 
cessive closure of different arterial branches, but in these 
the paralysis of the tongue and lower part of the face is 
much more irregular than it is in the case of the cerebral 
lesions. The distribution of the symptoms in these cases 
is indeed so irregular as to make it almost impossible to 
give any general description of them, and this very irregu- 
larity constitutes their most important distinguishing feat- 
ure. In the cases in which the symptoms are not irregular, 



84 BULBAR PARALYSIS. 

their symmetry is generally conspicuous from the first, for 
the reason that I have explained, — because the nuclei on 
both sides receive their blood from the branches of a vessel 
on one side. But diagnosis of the precise nature of the 
sudden vascular lesion which causes the symptoms is often 
a difficult matter. When there is syphilitic disease of the 
whole of the vessel from which the nutritive branches pro- 
ceed, the recognition of the fact is indeed seldom difficult. 
It is determined by the same evidence which enables us to 
recognise such disease in other arteries, and therefore need 
not detain us now. Embolism we may also dismiss as rare 
in this region, and associated with a distinct source of the 
obstructing plug. But the point of chief difficult}', and also 
of chief importance, is the determination of the question 
whether a senile lesion is hemorrhage, or softening from 
atheromatous thrombosis. The latter process is the com- 
mon one here, and it may be safely assumed when the 
symptoms come on in several distinct attacks, as was the 
case in the patient before us. But the difficulty is rendered 
greater by the fact that a good many cases which have 
been described as hemorrhage have really been cases of 
arterial occlusion with secondary extravasations in the 
affected region. The distinction of such a lesion, in its 
early stage, from a primary hemorrhage, is not easy when 
the affected areas are small. A hemorrhage which is suf- 
ficiently extensive to cause considerable paralysis would 
certainly give rise to severe initial symptoms, and if these 
are absent it is justifiable to assume atheromatous throm- 
bosis rather than the rupture of an artery. 

The prognosis and course of the sudden and the chronic 
forms of necessity present a considerable difference. The 
chronic form, at whatever age it occurs, has a progressive 
tendency, and as long as the symptoms continue to increase 
serious anxiety cannot but be felt regarding the issue. 
Many cases of this description end fatally in one or two 



ELEMENTS OF PROGNOSIS. 85 

years from the onset. But in this disease, as in analogous 
progressive muscular atrophy, there is a marked tendency 
for the progress of the lesion to undergo arrest after it has 
reached a considerable degree of intensity, and has produced 
so much damage that the state in which the patient is left 
is pitiable. It seems to be the case in the patient before 
you, in whom the malady seems no longer to be increasing. 
The prognosis is certainly worse in a case in which the dis- 
ease of the medulla supervenes on degeneration in the spinal 
cord, and bulbar paralysis is thus added to pre-existing 
muscular atrophy. It is worse, moreover, in the cases in 
which the symptoms are extensive and involve the parts 
concerned in swallowing as well as in articulation, the 
pharynx as well as the tongue and lips, than in the cases in 
which, as in this patient, only the structures for articulation 
are each affected. But of necessity the prognosis may have 
to be modified by the state of the larynx, and by the ten- 
dency there may be for particles of food to pass into the 
glottis and trachea. The chronic inflammation of the lungs, 
which is thus produced, is one of the most common causes 
of death, and when this source of danger exists the pros- 
pect of life being long preserved is always considerably les- 
sened. From the larynx the chief risk is that which arises 
from the occasional paralysis of the abductors of the vocal 
cords on each side. In this patient, fortunately, such par- 
alysis exists on one side only, and so all its characteristic 
indications are absent, with them the danger which bilat- 
eral paralysis always involves. When both cords are close 
together — so close together that the inrush of air inbreath- 
ing gives rise to inspiratory stridor — the danger of suffoca- 
tion from slight catarrhal swelling of the cords is, as I have 
said, extreme, and adds much to the gravity of the case. 

In the acute form, if the onset is survived, some degree 
of improvement maybe confidently anticipated, and it may 
be expected to go on for a considerable time. The chief 



86 BULBAR PARALYSIS. 

danger arises from the existence of conditions favoring 
other attacks ; it varies according to the probable amount 
of disease in this and other cerebral arteries, and is also in- 
fluenced by the extent to which other influences have co- 
operated in producing the obstruction. It is governed by 
the same rules as similar softening in other parts of the 
brain, and I need not advert to it here. The danger of later 
extension is never entirely absent in atheroma, and even in 
the case of syphilitic disease it may continue for some time. 
The cicatricial process in the wall of the diseased artery, by 
which the disease is removed under the influence of treat- 
ment, may involve the formation of fibrous tissue in the 
wall, which goes on contracting, and this may entail the 
closure of some other small branch, months after the occur- 
rence of the primary lesion, and after the disease of the 
wall has yielded to the influence of the drugs which are 
administered. Thus in all cases of sudden bulbar paralysis, 
the prognosis should be tinged with caution, and sometimes, 
even after the onset is survived, with distinct concern. 

The rare cases of acute inflammation, in which the symp- 
toms develop in the course of a few weeks, must at present 
be regarded as very serious. Ignorant of its causes, we are 
without the means of arresting the morbid process, which, 
in most of the few cases hitherto observed, has gone on to 
a fatal termination. But the probability that the process is 
due to a toxic influence is very great, and here also we may 
hope that the future will soon bring that which the present 
does not afford, and that we shall not have long to wait 
before we obtain the means of arresting the disease, and of 
doing so before the change in the nerve elements has pro- 
ceeded to a degree that precludes their recovery. 

You will have gathered from what I have said that the 
treatment of bulbar paralysis is one of the gloomy regions 
of the therapeutics of the nervous system. It is a subject 
on which there is, unfortunately, only too little to say. 



TREATMENT. 87 

That of the sudden form does not differ in any material 
point from the treatment of similar vascular lesions in other 
parts of the brain. When the sudden paralysis is followed 
by loss of faradic irritability, with preservation of voltaic 
irritability, that is, the reaction of degeneration, it is desir- 
able for a time to keep up the irritability of the muscular 
fibres by the application of voltaism in any part to which 
electricity can be applied, in the hope that the nuclei from 
which the degenerated nerves proceed may be only dam- 
aged and not destroyed, and that recovery, with regenera- 
tion of the nerves, may ultimately occur. In such a case 
we follow, therefore, the same rule which would guide us in 
the treatment of an acute lesion of the motor grey matter 
of the spinal cord, and endeavour to keep the muscles in as 
good a condition as possible, in case the motor impulses 
should ultimately be again able to reach them and to act 
upon them. 

In the chronic form, which occurs in the old, treatment 
directed to the morbid process seems to be entirely useless. 
The disease is a local senile change, and as such is beyond 
the reach of any influence we can bring to bear upon it or 
which the future is likely to afford us. The facts at present 
available regarding the chronic forms, which occur at 
earlier periods of life, suggest the same correspondence 
with analogous affections of the spinal cord and a similar 
practical application of the correspondence. In the form 
in which the muscles waste, the hypodermic injection of 
strychnine, of unquestionable service in the spinal affection, 
should always have a thorough trial. There is no reason 
why it should not be effective in the atrophic bulbar paral- 
ysis as well as in " progressive " muscular atrophy. Its 
use is not contra-indicated by previous administration by 
the mouth, and should not be delayed, because, if arrest 
can be obtained before the malady is advanced, even if im- 
provement is not secured, the condition of the patient is far 



88 BULBAR PARALYSIS. 

better than if the disease had obliterated most of his power 
of articulation, and some of his ability to swallow. The 
danger of pulmonary consequences, which result from the 
latter, must also be kept in mind in the treatment of every 
form of bulbar palsy, and every expedient, such as slow, 
deliberate eating, and food in a semi-solid form, which may 
lessen the chance of the entrance of particles into the trachea, 
and thence into the bronchi, should be insisted on. By 
these means, death may be averted or postponed more fre- 
quently than we can perceive. I have unfortunately not 
found anything effective in diminishing the flow of saliva, 
which is so great a trouble to many patients. 

In general management, do not forget that the sufferers 
are often much distressed by the inability to make them- 
selves understood ; endeavor to lessen this as far as you 
can, by persuading them to express themselves in writing 
rather than by efforts to speak, which only end in failure, 
and involve a strain on the affected structures which cannot 
be other than injurious. 



LECTURE VI. 
FACIAL PARALYSIS. 

Gentlemen : — Complete paralysis of the right side of the 
face, in a child of seven, who presents no other symptoms, 
— that is the problem before us. You have heard the 
questions asked, and the answers given by the child's 
mother, and that we found no evidence of a cause ; you 
heard the mother give a negative answer to every inquiry, 
— there had been no blow, no exposure to cold, no dis- 
charge from the ear. Those are the three chief causal facts 
to be sought in every case. Even pain in the region of the 
nerve was denied. But one other question was asked that 
should never be omitted in such a case : Has the child suf- 
fered from earache ? The mother then remembered the fact 
that had been forgotten, remembered it with surprise, so 
little had she thought it connected with the affection of 
the face. 

You see the symptoms which the child now presents, 
and you have heard the story of the onset.* You see that 
the face is symmetrical at rest, but in movement all sym- 
metry is lost in the distortion produced by the limitation to 
one side of all the familiar movements that the will can 
cause, or by which emotion is expressed. There is no 
movement, voluntary or emotional, in any part of the face. 

Paralysis of all the muscles supplied by the facial nerve, 
on one side only, and without other symptoms, always 
means disease of the nerve trunk. Practically, moreover, 

Clinical Journal, February 14, 1 894. 

* From a report by Mr. H. Caiger. 

89 



90 FACIAL PARALYSIS. 

if it occurs without obvious disease or injury near the nerve 
after it emerges, it means disease of the nerve during its 
passage through the bone. These two facts should be 
fixed in your mind, and the reasons for the conclusion 
should also be clearly understood. Never learn a diag- 
nostic rule, indeed, never accept any general assertion, 
without also endeavouring to ascertain on what the rule 
depends, or the assertion rests. Unreasoned conclusions 
are the bane of students. Without the facts to make them 
cohere with our previous knowledge, such conclusions will 
soon slip from the memory, or if they do happen to be 
retained, it is only by dint of pressure which alters their 
form, or drives them into some place to which they do not 
properly belong. They are remembered wrongly, and do 
you more harm than good. But fix the assertions by their 
evidence, the rules by their reasons, and not only do they 
remain, but they take root, and they become part of your 
real knowledge and a source of increasing power. 

You are no doubt familiar with the distinction between 
the two chief forms of paralysis of facial muscles, — the 
general palsy of all parts which is often, as here, absolute, 
and the form in which only the lower part of the face is 
involved, which is never absolute. The first, as you know, 
means disease of the nerve, or of the nucleus from which 
the nerve comes, while the other (so common as part of 
hemiplegia) generally means disease of the cerebral hemis- 
phere, and always means disease of the path between the 
cortex and the nucleus, or disease of the cortex itself. 
Hence the latter is sometimes called cerebral facial palsy, 
but this is not an accurate term, because this form may 
result from disease in the crus, or in the upper part of the 
pons. A more accurate name, therefore, and one by no 
means inconvenient, is supra nuclear palsy. On the other 
hand, the general palsy of the face may be either nuclear 
or infra-nuclear. It is often called " peripheral," but here 



STEPS OF ADVANCING SCIENCE. 



91 



again we have a word which it is wise to avoid. If it does 
not mislead, it is liable to distort a student's first concep- 
tions. Such distortion involves a waste of mental effort, 
since it has to be rectified. The "periphery" properly 
means the distal extremity ; " peripheral palsy " should be 
due to disease of nerve-endings — such paralysis as many 
poisons produce, not rarely, in other parts. But the word 
is not used in that sense in reference to the face. It is used 
to mean disease of the fibres anywhere in the course of the 
facial nerve, and even palsy that is produced by a lesion of 
the nucleus within the pons ; that is of the central origin 
of the nerve, is sometimes spoken of as "peripheral." 

This point, — the use of the word " peripheral " in connec- 
tion with palsy of the face, may excuse a digression for a 
moment, to note an illustration of that oscillation of opinion 
that always attends advancing knowledge. The truth of 
yesterday may be untrue to-day and true again to-morrow. 
The grounds of an induction may become insecure when 
we know the facts more thoroughly, and yet, again, new 
facts may re-establish that which seemed exploded. When 
many of those who now teach, first studied medicine, they 
were taught that the nerve endings are the seat of the lesion 
in the commonest forms of facial palsy — that which follows 
exposure of the side of the head to cold. The cold, acting 
on the surface, was assumed to act on the nerve endings in 
the muscles of the face and thus to cause the paralysis. 
The same explanation was given of other palsies following 
an exposure to cold, such as the local atrophic palsy of 
children, "infantile paralysis." This pathology was purely 
hypothetical ; no evidence of it had been ascertained, and 
there was no demonstrable analogy that could be produced 
to support it. Indeed, it now seems to us strange that the 
opinion should have been accepted so generally, since a 
little consideration will show how great a difficulty there 
must always have been in adjusting it to the facts. Why 



92 FACIAL PARALYSIS. 

should cold act upon the extremities of one nerve, upon all 
of them up to the middle line, and no further, not a single 
muscle or fibre on the other side? Why should the effect 
of cold acting on the surface be absolutely limited to the 
endings of one nerve? This difficulty does not seem ever 
to have been recognised. When increasing precision of 
observation, and a wider comparison of facts, suggested 
irresistibly that such a paralysis must be due to a process 
acting on the fibres where all are near together, or on the 
contiguous structures from which they come, and when it 
was discovered that the latter was the true pathology of 
infantile palsy, the idea that disease of nerve endings was a 
cause of paralysis disappeared. All such palsies were 
ascribed to disease of the centre or nerve trunk. Again, 
new facts came, and have compelled a partial reversion to 
the old opinion, that a primary affection of the terminal 
parts of nerves is a frequent cause of palsy. But it is 
chiefly in the limbs that we find evidence of this. We 
have, indeed, returned to this opinion in some cases of 
paralysis of the face, but we have not returned to it as an 
explanation of the palsy that is limited to one side of the 
face, and for which it was once considered the adequate 
explanation. It is very unlikely, however the pathological 
pendulum may swing under the impulses of new discov- 
eries, that we shall ever find reason to think that such palsy 
as you see before you in this child, is ever the result of 
disease of the nerve endings. We shall presently note the 
significance of this. 

Let us return to the two main forms and their distinc- 
tions — the infra-nuclear palsy which is often complete, and 
the supra-nuclear palsy that is never complete. You per- 
haps know the hypothesis by which the difference is ex- 
plained ; it is indeed somewhat more than a mere hypothe- 
sis. In proportion as muscles act together on two sides, 
the muscle on each side is represented in both hemispheres 



DIAGNOSIS OF COMPLETE PALSY. 93 

of the brain ; that is, either hemisphere can act on the mus- 
cles of both sides. Hence, in disease of one hemisphere 
of the cortical centre, or the path from that centre, the 
muscles escape in proportion to their bilateral association. 
When I say they escape, I ought to say they either escape, 
or they suffer only at first. They may be affected for a few 
days, but the initial weakness soon passes away, at least 
in great measure. Apparently the structural arrangements 
by which the hemisphere acts on those muscles on its own 
side are only slightly in habitual use, but their functional 
capacity quickly increases. This point, however, is one 
that we must consider another day; it would lead us too 
far from our present subject. It is the complete palsy — 
complete in range — of which an instance is before us, with 
which we are now concerned. 

We can carry the diagnosis beyond that of the exclusion 
of supra-nuclear disease. Paralysis of all parts of the face, 
if it exists alone and is on one side only, means disease of 
the nerve after it has left the cranial cavity. Theoretically 
it does not ; the whole nerve might be affected alone within 
the skull. But, as a matter of experience, it is not. The 
statement I have made is true in fact. Further, if there is 
no indication of a cause acting on the nerve after it has 
emerged from the canal in which it passes through the 
bone, such a paralysis means disease of the nerve within 
this canal. 

This conclusion is, I need not say, of the utmost practi- 
cal importance. In a large number of cases of facial palsy 
— in the majority indeed — it takes us at once to the seat 
of the disease. But to be able to use such a diagnostic 
rule you must know its reasons. Without a knowledge of 
the reasons few such rules are useful, because you cannot 
feel so sure of their validity as you must feel if you are to 
employ them with the confidence that is essential. You 
cannot feel sure that there are no exceptions, unless you 



94 FACIAL PARALYSIS. 

realise why there cannot be exceptions. The facts on 
which this rule is based are these : — First, there are two 
portions of the nerve which cannot suffer alone on one side 
only : these parts are the beginning of the fibres and their 
terminations — the cells from which they spring, and the 
structure in which they end within the muscle. These 
parts are so situated that all of those of one nerve cannot 
be affected on one side and alone. The nerve cells occupy 
a considerable area of the pons, and those for the muscles 
of the eyelids ?,:t some distance from those for the lips. 
The cells are adjacent to other important structures. Hence, 
the whole of the nucleus cannot be damaged by one lesion, 
so as to affect all parts ::' the face without other structures 
suffering, and suffering in such a manner as to give rise to 
obtrusive symptoms. Moreover, this is true not only of 
the nucleus, but also of the fibres proceeding from i: di 
their passage through the pons. All the feres : f the nerve 
are never damaged within the pons without adjacent struc- 
tures being alsc damaged soas to cause conspicuous symp- 
toms. Thus the isolation of the paralysis of the face, the 
affection of the whole of one nerve and of that only, ex- 
cludes an organic lesion within the pons. 

The nerve-cells may suffer, and may have their function 
abolished apart from what is commonly termed an organic 
lesion. They may cease to act in consequence of a degen- 
erative process, or in consequence of the influence of a 
toxic agent. This is true, also, as I have already intimated 
t: you, of the other extremity of nerve fibres — their ter- 
mination within the muscles. These are now known to be 
occasionally the seat : ■:' degenerative processes, and they 
are also known to be the parts influenced by certain 
poisons. But such agents do not act only on the nerve 
endings of one side. The reason for this is important, and, 
as I just now said, must be specially noted. It is a general 
law of extreme importance. The same structures on the 



AN IMPORTANT GENERAL LAW. 95 

two sides possess the same pathological susceptibilities. 
They suffer together in degenerative processes, and they 
suffer together under toxic influences, whether these be 
what we commonly term poisons or whether they are only 
seen in what we call diseases. Thus both sides of the face 
may be paralysed throughout as part of diphtheritic par- 
alysis, and as part of multiple neuritis, due to some toxic 
agency, — but one side of the face never suffers alone. This 
is the point to which I adverted in speaking of the theory 
that cold acts on the extremity of the fibres. Our present 
knowledge shows that it could not affect the terminations 
of all the nerves on one side and none of those on the 
other. Such a cause must, if it acts on the extremities of 
the nerves, cause bilateral paralysis. As a fact, it does so. 
Remember, then, in all parts of the nervous system, and in 
relation to all cases of the character I have mentioned — 
those due to degenerative processes and to toxic influ- 
ences — the effect is bilateral ; and a complete palsy of 
any part on one side practically excludes such general 
causes. 

The law which underlies these facts, therefore, may be 
expressed thus : A palsy which is directly due to a 
general cause is bilateral ; conversely, a bilateral palsy 
indicates a general constitutional influence. A unilateral 
palsy is due to a local cause ; it is not the direct result of a 
general process. I use the word "direct" result in order 
to be strictly accurate. The meaning of the restriction is 
this. The direct effects of general causes are due to their 
action on the nerve elements themselves ; but general 
states sometimes cause local effects by acting on the 
vascular system, or they may predispose all parts to suffer 
from an influence which acts only on one. Moreover, a 
unilateral palsy means a process which begins outside the 
nerve elements and affects them secondarily. That is a 
most important general law, applicable to all parts of the 



96 FACIAL PARALYSIS. 

nervous system — most important to remember in all cir- 
cumstances and in all localities. 

Next, the limitation of the palsy excludes disease of the 
nerve within the skull. After it has left the pons, a process 
outside the nerve fibres cannot reach a considerable decree 
and affect the facial nerve alone. The auditory nerve is 
contiguous to it from the surface of the pons to the bottom 
of the internal auditory meatus, and a process external to 
the facial nerve, sufficiently severe to paralyse it com- 
pletely and in all its parts, must affect the auditory 
nerve as well ; often it affects other nerves that are 
in the neighborhood. On the other hand, a cause 
acting on the facial nerve after it has passed through 
the skull will be conspicuous ; it is always an injury or a 
considerable local inflammation, and, in either case, is 
obvious. Hence, therefore, you can now understand the 
foundation of the important diagnostic rule which I laid 
down before : that a complete unilateral palsy of the face, 
without other symptoms, must mean disease of the nerve 
as it passes through the bone. 

The diagnostic problem is thus narrowed in regard to 
the seat of the lesion, and this facilitates the process of 
diagnosis even more than may at first sight appear. We 
cannot, indeed, carry further the process of exact localisa- 
tion, except that, if the short length of nerve which inter- 
venes between the origin from it of the vidian above and 
the chorda tympani below, is affected, taste is lost on the 
side of the tongue in front. But this is of little real value, 
because a morbid process may begin at one spot and may 
spread through a considerable extent of the nerve. The 
state of the palate gives us no localising information. 
Paralysis of the palate is never produced by disease of the 
facial nerve. The belief that it is so is one of those curious 
pathological myths which have arisen from the misinterpre- 
tation of what may be termed normal abnormalities, if you 



NATURE OF THE LESION. 97 

will forgive the expression — deviations from perfect sym- 
metry, which have no significance for us except in so far as 
they may lead us into error. 

But the special aid in diagnosis which we derive from 
this restriction of a morbid process to the part of the nerve 
which lies in the narrow winding canal in which it passes 
through the temporal bone, is due to the aid it gives in the 
next step in diagnosis — the step which is of chief practical 
importance, the nature of the lesion of the nerve. In this 
part of its course the nerve suffers from only three morbid 
processes, and of these three one can be excluded without 
difficulty. The processes are: — (1) primary inflammation 
of the sheath and interstitial tissue, which is the cause by 
which the most common form is produced, that which is 
due to cold ; (2) the spread to the nerve of inflammation 
due to ear-disease; (3) its compression or destruction in 
consequence of a growth in the bone. It is the last of these 
which may safely be put on one side unless there are other 
obtrusive indications of a growth, because it is a very rare 
cause, and not to be thought of unless such indications 
exist. 

The diagnosis between the two forms of inflammation, 
that which is communicated from the ear, and that which 
is primary (the so-called " rheumatic " form), is seldom 
difficult. They differ in the period of life at which they 
chiefly occur; although each may be met with at any age, 
ear-disease is a rare cause except in childhood, while 
primary neuritis is seldom met with till childhood is over. 
Moreover, the mischief in the ear which spreads to the 
nerve is generally considerable in degree and in duration. 
In most cases there is actual disease of the bone, and it is 
the progress of the caries that brings the associated inflam- 
mation into such proximity to the nerve that this becomes 
affected. In such disease there is almost invariably per- 
foration of the tympanum and a constant discharge from 
9 



98 FACIAL PARALYSIS. 

the ear. If there is no history of discharge, disease of the 
ear is not likely to be the cause. But this rule, true of 
facial paralysis in general, is not invariably true of it. 
Exceptions are met with, and this case is an illustration of 
the fact. We often hear vaguely of exceptions which 
" prove " or " test " the rule. The rules to which this say- 
ing is applicable are in most cases general rules ; they are 
laws that are true of the majority of instances which come 
under them ; if these are separated and scrutinised, it will 
be found that the exceptions occur under special condi- 
tions, and that these special conditions have been ignored 
in formulating the general statement. We have to be 
chiefly guided by the majority of cases, but we should 
recognise the existence of exceptions, and know when they 
may occur, that we may search for their indications if we 
have any reason to suspect an exception to our rule. If 
we attempt always to give weight to them, such weight as 
we give to the majority, we shall be in constant uncertainty. 
Indeed, it is not unlikely that we may come to the con- 
clusion, as a distinguished scientific man remarked to me 
of the impression left on him by one of the most famous 
teachers of his early days, that " no sane man could make 
a diagnosis." 

The exception to the rule that obtrusive signs of caries 
long precede the facial paralysis which results from otitis, 
depends upon the anatomical conditions of the ear. This 
has not indeed been actually proved, but we know that 
exceptional conditions often exist ; they explain that which 
would be otherwise inexplicable, and which nothing else 
explains. In some cases, fortunately not common, the 
facial nerve is separated from the tympanic cavity by a 
layer of bone so thin that inflammation can readily pass 
from the cavity to the nerve sheath. In such, bone disease 
is not necessary for the extension of inflammation to the 
nerve. 



A SIMPLE SOURCE OF ERROR. 99 

You can now understand why I asked so carefully about 
the earache. It is not enough to ask if there has been 
discharge. Discharge generally means disease of bone : 
disease of bone is the common cause of secondary facial 
paralysis, but the nerve is sometimes affected by extension 
when there is no bone disease. This case seems to be of 
that character, and hence, I am anxious to impress its facts 
upon you. It is an illustration of one of the two chief 
simple sources of error in diagnosis, not seeing the com- 
mon, not knowing the rare. I say simple causes as 
opposed to the more complex sources of error in rea- 
soning. 

This is an instance of the rare; it is an example of the 
occurrence of facial neuritis by extension from the middle 
ear, without bone disease. It is exceptional, because it 
must depend on exceptional conditions. A " passage " of 
inflammation implies a way for it to pass out. Normally, 
there is no way free enough for the passage of simple in- 
flammation. But simple inflammation may spread from 
the lining membrane of the tympanum to the nerve, when 
the layer of bone which separates the tympanic cavity and 
the nerve is thin. Indeed not only may it be thin, it may 
be even actually deficient. Inflammation not only may, 
but, if considerable, must then spread to the nerve. Ves- 
sels also pass through the bone, and by these an intense 
inflammation may pass ; but it is doubtful whether a 
simple catarrhal inflammation, such as this child seems to 
have had, would do so, if the conditions were normal. 

One other point, and that of great importance, the case 
also illustrates. The earache of children is almost always 
due to inflammation of the middle ear. Most of you 
know its character from the recollections of childhood, 
for few children escape some attack, and the peculiarity of 
the pain impresses itself on the memory. It is one of the 
maladies that may be called " domestic diseases " ; few 



ioo FACIAL PARALYSIS. 

mothers dream of sending for medical assistance for what 
they are pleased to call " simple earache." But between 
the earache which lasts a few hours and then passes off, 
and the earache which is the prelude to a suppurative in- 
flamation, there is every gradation. There seems to be 
no difference in the character of the pain. 

It is important to remember this. It is one of the facts 
that should be part of the education of the mother — one of 
the many facts that might, with great advantage, replace 
the rubbish that has drifted into the maternal mind: by no 
means harmless in the minds of the many persons who "get 
on much better without a doctor." I lately saw a child with 
infantile palsy of one leg. This leg had suddenly become 
powerless. The mother — with no excuse of poverty or 
station — consulted her female friends, and, resting content 
with their assurance that it was " only the teething," and 
that "the leg would soon get all right again," allowed five 
whole months of utter immobility to pass before she 
thought it necessary to ask her doctor to look at the 
child's leg. And many cases of suppuration in the ear 
and of disease of the bone are due to neglect of the warn- 
ing of simple earache. 

In the case of children who are liable to earache, great 
care should be taken to guard against exposure of this 
part of the head to cold, and especially to cold east winds ; 
and still greater care should be taken to get rid of an 
attack as soon as possible. How seldom are the lessons 
learned that are, nevertheless, familiar in proverbial form, 
such as that embodied in the adage about the " stitch in 
time." We could wish the statement were literally true, 
and that the absence of early treatment, which so often 
would cut short a grave disease, could be made up for by 
the amount represented by the multiplier of the proverb. 

If you take all the nerves of the body, and consider the 
frequency in which they are so diseased as to cause symp- 



OBSCURE CAUSES. 101 

toms, I think the fifth, the sciatic, the ocular, and the facial 
nerve would be their order. The reason for the frequency 
of facial paralysis is not yet entirely understood. We can 
understand, however, why it is so obtrusive when it does 
occur. It is manifested with peculiar readiness, because 
outward swelling is prevented by the rigid walls of the 
canal. Hence the inflammatory effusion compresses the 
nerve fibres, and at once interrupts the conduction of the 
motor impulses, quickly causing inability to move the 
facial muscles. But this, although it explains the fact that 
even a slight inflammation causes considerable palsy, leaves 
its actual frequency still mysterious. Paralysis of this 
nerve from cold is certainly more common than we should 
anticipate, considering that other nerves are not less exposed. 
Perhaps the cause is to be found in some conditions of 
the circulation within the canal, in consequence of which a 
congestion that would otherwise be transient and harmless, 
leads to undue stasis, and becomes an actual inflammation 
with all its grave results. 

The more remote causes of the primary neuritis are 
obscure. It is occasionally associated with the diathesis 
that causes fibrous and muscular rheumatism, and which is 
probably not far removed from that which causes or results 
from gout. I have twice known a patient to have facial 
neuritis at one time, and at another an analogous rheu- 
matic inflammation of all the nerves at the back of the 
orbit. Remember, too, that what we call fibrous rheuma- 
tism is probably also not very different from an inflamma- 
tion. Certain it is that this still mysterious muscular 
rheumatism may become inflammation. Many cases of 
sciatic neuritis, certain and severe, arise by the traceable 
extension, along the fasciae to the sciatic notch, of a pri- 
mary lumbago. 

We will not attempt to ascertain, in this child, the electri- 
cal irritability of the muscles. We know what condition 



102 FACIAL PARALYSIS. 

we should find. No complete paralysis of a motor nerve 
continues for a month without the nerve fibres degenerat- 
ing below the lesion, and there is always loss of all irrita- 
bility of the nerve trunk, loss of the faradic irritability of 
the muscles, and increased irritability of the muscular 
fibres to voltasim. We should learn nothing by the exam- 
ination, and you have frequent opportunities for observing 
the facts. Without doing good to ourselves, we may do 
harm to the patient. The paralysed muscles will need 
electrical stimulation, and in the case of children it is neces- 
sary to be extremely careful in the application of electricity. 
If you so use it as to cause pain the child will be fright- 
ened, and will dread each therapeutical application. Once 
thoroughly frightened, a child seldom loses the dread, and 
no child can endure a frequent distressing emotion without 
harm. If care is taken, all that is needed, or almost all, 
can be achieved without the production of any of this 
injurious alarm. But to secure this result the first applica- 
tion must be so feeble that no new sensation is produced. 
Indeed, it is well, the first time, not to allow the current to 
be strong enough to be felt. Then, if the current is grad- 
ually increased in strength in successive applications, after 
a few days a strength may be used that will make the mus- 
cles contract visibly without eliciting a tear. It is surpris- 
ing how strong a current children will bear if this plan is 
adopted. For the same reason you should never use the 
faradic "current" in the case of young children. Move 
the hammer with your fingers instead of permitting it to 
oscillate automatically. The less frequent momentary cur- 
rents will cause a muscle to contract with merely a pecu- 
liar shock-like sensation, devoid of pain. If you use the 
repeatedly recurring shocks, produced by the automatic 
interruption, a painful stimulation of the sensory fibres is 
produced, even with a lower current than will cause the 
muscles to contract. The difference, in the case of child- 



AIDS TO PROGNOSIS. 103 

ren, is of great importance, for the reason I have men- 
tioned. For the same reason, also, if you find it impossible 
to cause visible contraction of the muscles without produc- 
ing distress, be content with a little weaker current. I 
cannot understand the prevalence of the notion that in any 
therapeutic procedure, with drugs, electricity, or any other 
agency, no good is done unless a certain physiological 
effect is produced. Surely the production of a manifest 
effect is only a question of degree. If a certain strength 
of current cause a visible contraction of a muscle, it does 
so by making a large number of the fibres contract with 
sufficient energy for the effect to be seen. Are we to 
assume that a current just below this strength causes no 
contraction because we cannot see the whole muscle 
shorten ? There must be contraction of the fibres before 
we reach that degree which causes visible movement, and 
it is surely impossible that this stimulation can be without 
the influence on the nutrition of the fibres, and on the 
maintenance of their irritability, which the stronger current 
has. On the contrary, the consideration of the fact sug- 
gests distinctly that such a weaker current only needs to 
be continued for a longer time to do all that the stronger 
current can do. Remember, all that electricity can do in 
such cases is that which I have mentioned. We have no 
reason to believe that it has any influence on the nerve 
fibres ; it does seem to keep the muscles in a better con- 
dition for the nerve impulses to act upon them when con- 
duction is restored, and to enable them to respond better 
to the motor influences when these can again reach them. 
Hence, in all cases in which the paralysis is complete, or 
considerable, for more than two or three weeks, it is desir- 
able to employ electricity. 

Moreover, we do not here need an electrical examina- 
tion to assist in forming a prognosis. This is, it is true, 
one of the most important services electricity renders in 



104 FACIAL PARALYSIS. 

such cases. It is surprising to those who cannot read its 
language, that of two cases of facial palsy alike complete 
and of the same duration, say two weeks, an electrical 
examination should enable a positive statement to be 
made that one case will be well in a fortnight, and that 
another will endure for months and will never completely 
pass away. And yet it is so. But we have other aids in 
prognosis. We can often draw conclusions of great value 
from the simple consideration of the conditions under 
which a malady developed, and, when a process in one 
place is due to extension from the same process elsewhere, 
the character of the primary symptoms is sometimes of 
significance. Here we have the fact that the paralysis re- 
sulted from an inflammation which was transient. The 
pain in the ear lasted only a few hours. Doubtless the 
process may have lasted longer, since when effusion and 
swelling occur, the pain of inflammation often lessens, but 
the duration of pain which is due to inflammation in the 
ear is of some value as a guide to the duration, and, there- 
fore, to the intensity, of the process. Thus judged, the 
process here was brief, and, being brief, was also slight ; 
for duration and degree are proportioned in acute inflam- 
mation. From this we may conclude that the inflam- 
mation of the nerve was probably only such a brief 
moderate process as would be limited to the sheath to 
which it first extended. The effects have already lasted 
a month, but before long some signs of improvement may 
be expected to occur. Over and above this, we have also 
the general law that cases of facial paralysis from ear dis- 
ease, on the whole, run a more favorable course than 
cases of facial paralysis from the primary neuritis. The 
reason for the average slighter severity of the affection is, 
perhaps, to be found in a more limited extent of the in- 
flammation. It is reasonable to assume that an inflamma- 
tion which is communicated will not affect so considerable 



TREATMENT. 105 

an extent of the nerve as one which is due to a primary 
process. 

In all such cases of facial paralysis the treatment must 
be twofold. Besides that suited to any recognisable con- 
stitutional state (which I assume you do not need to be 
told) we have to treat the primary disease of the ear, and 
we have to treat its consequence. In the case of ear dis- 
ease, this must first engage our attention, but the measures 
needful do not come within my own province to describe 
in detail. The most important, however, is unquestionably 
to afford a free exit to any pus which may have accumu- 
lated in the cavity of the tympanum, and to guard against 
any obstruction of such exit, including that which is pro- 
duced by non-absorbent cotton wool. Absorbent cotton 
wool changed two, three, or six times a day, according to 
the amount of discharge, is safe. The importance of 
cleansing by antiseptic washes you will have already 
learned. For the secondary inflammation of the nerve 
sheath we can do nothing directly, except by the applica- 
tion of counter-irritation. This is, indeed, the chief local 
measure in all cases, whether produced by cold or produced 
by extension. A blister should be applied over the mastoid 
process, and should be repeated as soon as the skin will 
permit. Never put a blister in front of the ear, over the 
place of exit of the nerve. You cannot blister without 
producing a little subcutaneous cellulitis, and I have known 
a trifling cellulitis in this situation to be a cause of facial 
paralysis — the inflammation reaching the nerve sheath, and 
spreading along it into the Fallopian canal. In all recent 
cases, moreover, hot fomentations applied over the ear and 
its neighborhood, constitute a very useful measure. They 
should be used for one quarter of every hour during the 
first day. We do not precisely know how hot fomenta- 
tions act, but it is certain that no measure has so potent an 



106 FACIAL PARALYSIS. 

influence on inflammation in its earliest stage. Probably 
the stimulation of the sensory nerves and the heat com- 
bined cause alternate contraction and dilatation of the 
vessels, which lessens the blood stasis. Perhaps, more- 
over, the nerve stimulation has some even more direct 
influence on the process of inflammation. But whatever 
the explanation, the fact is certain. 

The last element in the treatment is the application of 
electricity. This is only needed when the nerve fibres 
undergo degeneration. As long as the nerve retains any 
degree of excitability, and as long as the muscles contract 
when the induced or faradic current is applied to them, 
electricity is not needed. Its use is to keep up the nutri- 
tion of the muscles and to keep up their excitability. We 
have conclusive proof that it does the latter ; we have no 
proof that it does the former, because we do not find that 
the muscles to which it is applied waste less or waste more 
slowly than those to which it is not applied. But it is cer- 
tain that functional excitability cannot be maintained with- 
out nutrition being also influenced. You know the kind 
of electricity that should be applied. This is one of the 
elementary facts which every student learns or should learn 
as his first acquisition in the therapeutics of the nervous 
system. You must apply the kind of electricity to which 
the muscles respond, and this, as we have seen, is the 
voltaic current. You apply it in such a manner that it is 
interrupted, not frequently as the induced current is, but 
slowly, as by stroking down the muscle with one electrode, 
the positive or the negative, to whichever the muscle is 
most sensitive. It is not always the same, even when the 
nerves are degenerated. We interrupt slowly because, as 
far as we can judge, the element in the form of electricity 
which causes the difference in the reaction is one of time. 
Muscular tissue is much lower in the scale of excitable 



THE VOLTAIC CURRENT. 107 

tissues than is nerve tissue, and seems to be unable to 
respond to an electric current unless this has a duration 
considerably exceeding the very small fraction of a second 
which elapses before the automatic interruption stops the 
current of the induction coil. 



LECTURE VII. 
FACIAL CONTRACTION AFTER PALSY. 

Gentlemen : — When I asked your attention to the chief 
symptoms of facial paralysis, I had to leave for subsequent 
consideration the troublesome condition which accompanies 
return of power — the secondary state of contraction. It is 
not a trifling matter in many cases. It may be almost as 
great an evil as the original paralysis. It is, moreover, a 
subject of considerable interest, and its study throws light 
on other conditions. 

Observe carefully the face of the patient before you. 
The left side presents a slightly deeper naso-labial furrow 
than there is upon the right side. It would be natural for 
an observer to assume that the side on which the furrow 
is least marked is the weaker side, is that which was para- 
lysed. As a matter of fact, such an assumption is commonly 
made by students in such cases. The furrows of the face 
are determined by muscular action, and where furrows are 
less there is less muscular action, and therefore muscular 
weakness seems to exist. The impression is strengthened 
by the aspect of a gentle smile ; it is not easy to obtain it — 
the attempt often results in no movement, or in one that is 
much in excess of " gentle." But the request for one, 
cautiously put, often obtains what is desired. You see it 
does so here. You see that the gentle movement is dis- 
tinctly greater on the side of the deeper furrow, and the 
smile thus seems to confirm the opinion that there is more 
power of movement on this side. 

Clinical Journal, September 19, 1894. 
108 



ASSOCIATED MOVEMENTS. 109 

But our ability to excite emotion may be sufficient to 
make a patient laugh ; or we may obtain an energetic 
movement in elevation of the upper lip. In this you can 
see how much slighter the strong movement is on the side 
on which the slight movement was greatest. On the side 
of the deep furrow a slight movement is greater, but a 
strong movement is much less. Note, also, that when the 
eyes are tightly closed there is the same difference. An 
excessive degree of slight movement is associated with a 
diminished degree of strong movement. 

But you may have already observed for yourselves that 
there is more than this difference in degree. Even in the 
gentle smile you could not fail to see that the eyelids were 
more approximated on the side on which the slight move- 
ment was most considerable, and that this was conspicuous 
also with the stronger movement. It is very marked in 
the laugh. You know that emotional movement normally 
involves all parts of the face. The ocular fissure is nar- 
rowed in a laugh, the eyes may even be almost closed, 
while the angles of the mouth are drawn outward and up- 
ward by the zygomatic muscles in the ungraceful distortion 
of the face which custom makes us appreciate so keenly. 
This associated action is increased in the condition we are 
considering. With the increased readiness of action there 
is an increase in the associated action of the different parts. 
Moreover, with these there is associated the feature to 
which I first directed your attention — the muscular con- 
traction which deepens the furrows. This muscular con- 
traction is a persistent state ; it is accompanied by, and, 
indeed, I might say, illustrated and emphasised by occa- 
sional slight clonic contraction in the muscles, which you 
will have no difficulty in perceiving in this patient, if you 
presently carefully observe her. 

The furrows which come with years, sooner or later, are 
the result of the shortening of the muscles which have 



no FACIAL CONTRACTION AFTER PALSY. 

been most frequently employed in their varied uses, and 
especially in the expression of emotion, a shortening in- 
creasing with years and being increased in effect by the loss 
of elasticity of the skin. The emotions that are chiefly 
dominant impress their transient influence on the muscles 
by long repetition as a permanent effect. Everyone knows 
the varying expression which the furrows of age produce 
in the aspect of the face, and those who know the story of 
the life can often read it in the lines. Yet most persons 
remember instances which cannot altogether be thus ex- 
plained. We sometimes meet with a face which bears the 
aspect of sorrow as the sequel to a tranquil life, or see the 
furrows of a constant frown in one who is seldom angry, 
or the transverse frontal lines when surprise or concern has 
seldom been dominant. Of course, many of the lines which 
Time's fingers trace are due to that which is common to all 
persons, habitual movements which have only a little to do 
with emotion. The zygomatic muscles, for instance, are 
constantly employed otherwise than in the smile or in ex- 
pressing pain. Their contraction is the result of their 
habitual action, defectively opposed. But when all allow- 
ance is made for such influences, there remains much con- 
traction which we cannot explain except as the result of 
hereditary influence — the effect of emotion in past gener- 
ations, persisting to the present, and telling a story which is 
untrue of the present, but, like so much else that is myste- 
rious, is true of a perhaps distant past. It seems to be an 
indication of the continuity which makes our race extend 
unbroken, in all its variations, through time which we can- 
not estimate. 

The fact that the contracture which follows facial paral- 
ysis resembles in its effects the condition which age induces, 
renders its effect most distressing to the young. The con- 
tracture follows inevitably in every case of facial paralysis, 
with the exception of those which last but a few days. If 



DISTRESSING DISTORTION. in 

the paralysis is moderate, the contraction is moderate ; if 
severe, so is this sequel. If the time of life has come when 
lines are proper, then the contraction reproduces the due 
symmetry of the two sides of the face ; and if it does a 
little more, the excess is almost imperceptible. Although 
the associated overaction may cause a difference in the 
expression of emotion, unless there is energetic movement, 
the difference is slight. But that which is natural in age is 
unnatural in youth. The contraction produces its furrows 
in all periods of life, and the result in ybuth is that a face 
may one side correspond to the proper aspect of " sweet 
seventeen," and on the other to forty-five. The contrast is 
an evil as great as is the facial paralysis itself, and even 
greater. In the young, during the stage of palsy when the 
features are at rest, no difference is perceptible between the 
two sides, and it is only on movement that distortion occurs. 
But this late contraction causes a conspicuous contrast 
between the two sides, which is constant at rest. It is the 
more distressing because no hope can be held out that it 
will pass away. So keenly is it felt, that one patient of 
mine, a girl of eighteen, formerly epileptic and not of very 
stable mind, was so distressed at the daily reflection in the 
looking-glass, which she could not avoid, that she one day 
wrote a letter to me. It was to thank me for my efforts to 
do her good, but to say that she could bear it no longer, 
and that when the letter reached me she would be dead. 
The letter was to reach me on my visit to the hospital, and 
when it reached me it was true. 

In the old, however, the contraction is cosmetic in its 
influence. The early palsy obliterates the bilateral sym- 
metry, because it substitutes the smoothness of youth for 
the wrinkles of age, but the symmetry is restored by the 
late contraction. It is curious, by-the-by, to note how 
difficult it is for many persons who have long ceased to be 
young, to believe that the normal side of the face is not 



112 FACIAL CONTRACTION AFTER PALSY. 

that which is affected. In the early stage of the paralysis 
the smoothness of the affected side causes the furrows on 
the other, familiar as they are, to seem by contrast entirely 
strange. That which is so unseemly cannot be natural. 
They assume, therefore, that the side toward which the 
mouth is " drawn," is that which is affected. The convic- 
tion is not, as you might think, confined to one sex ; I will 
not say that it is not a little more common in one, but it is 
frequent enough in the other. A mirror has an interest 
for men as well as women. 

This late contraction, as I have told you, always follows 
facial paralysis except when very slight. It accompanies 
return of power, but only return of power that is incom- 
plete. This statement may surprise you. It implies that 
recovery of power is incomplete except in the slightest 
cases. You may have seen many cases of paralysis of the 
face which seem to have perfectly recovered. But you will 
find, on careful examination of the movements, that recov- 
ery is hardly ever perfect. You will find, also, that when 
you find any indication of contraction and associated over- 
action, you can always detect imperfect, power, however 
long it may be since the acute affection. Indeed, the over- 
action may be more conspicuous than the persistent defect ; 
but the defect is always there, although it may be incon- 
spicuous. In every organ and structure of the body the 
condition after inflammation is never as it was before. 
Could we perceive the minuter structure, we should be 
astonished at the degree of persistent change. In most 
parts the effect on function is not perceptible, because the 
function of the organ is manifested by the combined action 
of all its parts. Where each part has a separate function, 
the effect of persistent change is evident. This is so with 
the face. The evidence of imperfection is the greater the 
more pronounced the function, and the more delicate its 
adjustment. The face is the great vehicle of emotional 



A CASE OF BILATERAL PARALYSIS. 113 

expression. No pain or sense of pleasure comes and goes 
without a change in the state of contraction of the facial 
muscles, too slight perhaps to be analysed, but too definite 
to be unperceived. It is not surprising that an organ of 
expression so delicate should manifest the slightest inter- 
ference with the process of conduction of the impulses 
from the brain. 

This peculiar condition does not cause suffering. It 
may be attended with a sense of tightness in the face at the 
onset, but afterwards the patient is scarcely conscious of 
it, except when movement brings its presence to the mind. 
This, however, is not more than the patient quickly gets 
used to. The muscles in the lower part of the face on one 
side are, in general, adequately opposed by the action of 
those on the other side. If the second side should sub- 
sequently become paralysed, the contracture instantly 
becomes far more obtrusive both to the patient and to 
others. It is indeed very rare for the second side to suffer 
at a subsequent period, and very few instances are on 
record. A case lately came under my notice : A lady had 
been under my care five years ago for severe paralysis of 
the right side of the face, which had left considerable con- 
tracture. One day she was startled by finding a great 
increase in the contraction, and that there was deviation of 
the mouth considerable even on rest, greatly increased by 
movement. On looking in the glass, her previous expe- 
rience made it at once obvious to her that the left side had 
become paralysed. She came to London in a day or two, 
and the condition was very striking ; the vast increase in 
the effect of the old contraction, consequent on the loss of 
power on the other side, caused extreme distortion. For- 
tunately the attack proved brief, and in a fortnight the fresh 
palsy had passed away, and her state was as before. How 
far the quick recovery was due to the treatment adopted 
(which I have described to you before) or to the slightness 



U4 FACIAL CONTRACTION AFTER PALSY. 

of the inflammation, I cannot say. Remember that this is 
one of the maladies in which nine-tenths of that which can 
be done by treatment, can be done only during the first few 
days. It is one of the many diseases in which therapeutic 
knowledge on the part of the general practitioner, per- 
fectly ready for use, is of the utmost importance. Physi- 
cians are impressed perhaps unduly with this fact, because 
most of the patients who have reason to seek their subse- 
quent aid, are cases in which the needed treatment has not 
been forthcoming. It is impossible to overlook the room 
there is for more knowledge of the proper treatment of 
many diseases, knowledge which is such as to enable the 
necessary measures to be at once and confidently adopted. 
Practitioners, perhaps, do not adequately realize how large 
is the proportion of all possible good which they alone 
can do. 

I have dwelt at length on the features of this late con- 
traction because, trifling as it may seem to be, its practical 
importance is very great. As I said, although the annoy- 
ance occasioned by the paralysis may be greater in degree, 
it is almost always limited in its duration. That which is 
caused by the contracture is generally considerable in the 
first half of life, and it is not limited in its duration. It 
only ceases to annoy when the effect of years neutralizes, 
by balancing, its effect. Why it should be thus persistent 
will be seen if we endeavour to perceive something of its 
cause. 

Its cause is certainly the functional state of the nucleus 
of the nerve produced during the period of palsy. During 
the state of immobility a condition of the motor centre of 
the nerve has been induced by which a slight degree of 
excitation causes undue action, although the hindrance to 
conduction along the nerve is such as to lessen the total 
amount of energy which can be transmitted. It is not 
difficult to conceive that the narrowed fibres should have 



ITS CAUSE. 115 

their capacity for conduction restored so that they conduct 
perfectly a slight amount of nerve energy, and yet the 
amount of force they can conduct is permanently reduced. 
There is an explanation of this in the mode of conduction ; 
but I cannot now make it clear, because I should have to 
begin far, far back, in the elements of molecular physics. 

This state which follows paralysis is evidently due to a 
state of the motor elements of the nucleus, that is, the 
structures from which nerve energy is evolved. These act 
too readily, they act spontaneously so as to cause the twitch- 
ing, and they act on each other too readily, so as to pro- 
duce the associated overaction. The structures from which 
proceed the fibres for the different parts of the face, are 
connected in the nucleus, and these connections which 
subserve the normal associated action present in health a 
certain resistance, which limits this action. It is on this 
resistance, developed by normal function, that the due rela- 
tion of the associated action depends. That resistance 
becomes lessened during the palsy. It is lessened in con- 
sequence of overaction of the centre. Wherever we have 
overaction of nerve structures extending from one to 
another, the resistance between them is lessened, and the 
activity tends to increase the condition. It is as if the 
grooves in which wheels run are deepened into ruts, and 
the continued motion of the wheels precludes any diminu- 
tion in the depth of the ruts. It is as if a channel for water 
had become widened by the flow, and yet is inaccessible 
to any direct process of repair ; the constant flow of water 
through it precludes any natural reproduction of the 
natural resistance. So this overaction of the nerve centre, 
once set up, goes on. 

It is not difficult to perceive how it is probably set up. 
At least it is easy to see a mechanism that must inevitably 
have the result. Normally, the action of the central struc- 
tures of a motor nerve is regulated and restrained by 



u6 FACIAL CONTRACTION AFTER PALSY. 

impulses which reach the centre from the contracting fibres 
of the muscle by the afferent nerves, stimulated by the 
contraction of these muscular fibres. The voluntary and 
other impulses continually act on and excite the nucleus 
when the nerve is interrupted. In the absence of the con- 
trol which should be exerted on them by the afferent nerves 
from the muscles, this must lead to overaction of the nerve 
centre. Moreover, the obstruction in the nerve fibres can- 
not be without its influence in disordering the centre. 
Nerve fibres conduct by a process similar to, but less in 
degree than, that by which the nerve force is generated, 
and although we do not understand the process, we must 
conceive that the arrest of the transmission onward of the 
energy has an effect on the functional state of the centre. 
If the molecular changes of conduction cannot pass down 
the nerve, this passage into it must, after a time, be 
hindered, although the production force is not lessened. 
Hence also the abnormal action within the centre is 
increased. 

The occurrence of spontaneous twitching in the face is 
explained by the tendency to overaction on the part of the 
motor structures in the nucleus, and the fact that slight 
impulses of nerve force can pass readily through the nerve. 

I should like you to note the difference which there is 
between this form of contraction after paralysis and that 
which you meet with in the limbs. In these, the loss of 
power with changed reaction to electricity is often followed 
by muscular contraction, but the contraction is in the oppo- 
nents of the muscles that are paralysed, and not in these 
muscles themselves. It is due to the fact that the dimin- 
ished extension permits shortening. But the peculiarity of 
the contraction after facial paralysis is that it occurs in the 
muscles that are paralysed. The difference must be referred 
to the peculiar conditions which cause the loss of power. 
Nowhere else do we meet with so absolute an arrest of 



TREATMENT FUTILE. 117 

conduction in consequence of a lesion of the nerve which 
afterward lessens or almost recovers, as we do in the case 
of the facial nerve. It is, of course, due to the course of 
the nerve within the bony canal. Moreover, nowhere else 
have we the constant energetic influences from the brain 
exciting the motor centre, as in the case of the centre for 
the face. I have already dwelt on the peculiar relations of 
the face to emotion, which involve the constant excitation 
of the centre. The perfect bilateral association of the 
action of the two sides is another condition which precludes 
any cessation of the action of the brain upon it. It is very 
different with the spinal centres for the muscles which may 
be paralysed by disease of the nerves. Thus we can under- 
stand that the unique conditions of function and disease, in 
the case of facial paralysis, give rise to a condition here 
which we do not meet with elsewhere. 

You will perceive from what I have said that the condi- 
tion is beyond the influence of treatment. I have never been 
able to form an opinion on the question whether it lessens 
with time or not. If it does, the diminution is very slight. 
But there are three practical points connected with it. The 
first is that its advent is certain in all cases in which faradic 
irritability is lost or considerably reduced. Except in the 
very rare cases of absolute lasting atonic palsy, some power 
is always regained, but with it comes this sequel. Since it 
is annoying, it is always well to warn your patient that 
when the face recovers power, it will tend to overact, and 
that this is inevitable. Otherwise the patient is apt to think 
a fresh morbid state is coming on. When it begins, I think 
it well to stop electrical treatment. Its commencement co- 
incides with, or soon follows, the return of voluntary power. 
There is then enough power to influence the nutrition of 
the muscular fibres, and to render electrical excitation un- 
necessary. On the other hand, the stimulation of the sen- 
sory nerves by electricity tends, I think, by reflex action, 



1 1 S FACIAL CONTRACTION AFTER PALSY. 

to increase the contraction. The third point is the only 
measure which has, or can have, any influence. A trifling 
effect on it is probably exerted by what may be called 
"downward massage" of the face. The fingers should be 
drawn from the zygoma to the angle of the mouth repeat- 
edly, with gentle pressure, for a minute or two, several 
times daily. 

It is not pleasant to be able to advise so little. But, 
Gentlemen, remember this — it is true of ourselves and it is 
true of our patients — next to knowing what can be done 
and how to do it, the most important thing is to know what 
cannot be done. Sad, indeed, is the waste of time and 
money caused by efforts to get that which cannot be ; sad- 
der still is the waste of hope — hope created by baseless 
expectation — and the destruction of it that we call disap- 
pointment, disappointment that would not be were it not 
for the anticipations that have no justification. 



LECTURE VIII. 

ACLTE ASCENDING MYELITIS. 

G •:'■::'. ■:■■■:■:■: : — Be:": re '■■■t rr::ee: :: the spe:iai subject 
which ~e are :: ::ns:ier to-day, I cry::se :: describe :: 
you a case I saw last evening. There are many diseases 
which, because they are rare, or for other reasons, seldom 
come under the student's notice, and although description 
can never take the place of personal observation, it may be 
useful if the latter is impossible, and it may be the more 
useful if a case has been recently seen, and its facts are 
fresh and vivid in the narrator's mind. 

The patient whom I saw (with Dr. Parnell and Dr. Gray- 
ling, of Forest Hill) was a lad of 19, paralysed almost 
completely from head to foot, pale, with the distressing 
struggle for breath that comes when breathing power is 
getting less and less. The story of the case is as follows : — 

A month ago he had his first lapse from virtue, and the 
consequence was — not a rare one — an attack of gonorrhoea ; 
it was treated, and he recovered in a fortnight. He had 
not previously been in good health, having been over- 
worked at night A little more than three weeks after the 
onset of the gonorrhoea — about a week after its termination 
cays be:*: re I saw him — his le~s. :r.e fay, became 
weal-:, he scumbled : :: the stairs arte in a :e h: crs the weak- 
ness became considerable. The next day his abdominal 
muscles were feeble, and the legs oowerless, but with ex:es- 
sive knee-jerks (which disappeared two days later). On 

::•:*::..-: j':-wkz: I::-::: ::. :':-.}. 



120 ACUTE ASCENDING MYELITIS. 

weakness increased and extended during the next three 
days, and he became febrile. When I saw him last night 
his state was this : He was sitting, half upright, in a chair, 
breathing, as I have said, with difficulty, by means of his 
diaphragm and lower intercostal muscles, at the rate of 56 
respirations per minute, the deficiency in quantity of air 
inhaled having to be made up by increased frequency of 
respiration. His temperature was raised to 103 . His 
legs were absolutely powerless, without a trace of knee- 
jerk — flaccid palsy. From the right sole there was no 
reflex, but a touch on the left caused a considerable move- 
ment of the foot ; there was no abdominal reflex, but a 
stroke on the skin left the bright red line, lasting a long 
time, which shows acute disturbance of vascular innerva- 
tion. He could just flex his fingers, and that was all the 
movement left in his arms. The abdominal and trunk 
muscles were paralysed, except the lower third of the inter- 
costals and the diaphragm. The upper part of his thorax 
was motionless, and the sterno-mastoids were also power- 
less. He could swallow, and he could just speak, although 
with difficulty. The left side of his face moved less 
than the right; the left masseter contracted a little less 
than the right ; and movement of the eyes was accompanied 
with brief but wide nystagmus, greater on movement to 
the left side than to the right. Without any discoverable 
cause — without any hot application or the like — there had 
developed, within a few hours, a very large bulla over the 
inner side of the right ankle. 

It was thus a case of acute ascending paralysis, using the 
words in a symptomatic sense, and it had naturally been 
regarded as a case of that mysterious disease to which the 
term is specially appropriated, and which is also called 
"Landry's paralysis." I think that this reasonable conclu- 
sion is very near the truth ; but there was evidence of more 
than we have in that disease. Indeed, the case is particu- 



AN INSTRUCTIVE CASE. 121 

larly instructive from the point of diagnosis. " Acute 
ascending paralysis " depends apparently on a peculiar 
arrest of central, and perhaps peripheral function, by a 
peculiar blood state. In it there is no pyrexia ; the loss of 
function presents a perfect bilateral symmetry, never trans- 
gressed by such a deviation as the preservation of the 
plantar reflex on one side when it is lost on the other. The 
course of the symptoms is uniform, the knee-jerk is lost 
from the first, and never excessive at the beginning, as in 
this case. Although it is said that some parts may be 
passed over in the upward march of the palsy, as, in this 
patient, were the lower intercostal muscles, yet I think it is 
doubtful whether this is really true of Landry's paralysis, 
and whether the assertion has not been due to cases — such 
as this — which may so readily be mistaken for that affec- 
tion. The symptoms point to a derangement of the 
functions of the spinal cord, slightly but distinctly irregu- 
lar, both in time and place. There is no doubt that Landry's 
paralysis, as I have just said, is the effect of a toxaemic 
state on the nerve functions ; but all toxaemic conditions, 
in their isolated action, cause symmetrical arrest of func- 
tion; and the difference we had here in different parts and 
at different times, showed that there was an irregularity in 
the cause of the symptoms, — something more irregular 
than the simple inhibition of a blood state. The early ex- 
cess of the knee-jerk, together with the difference between 
the two plantar reflexes, and the nystagmus, pointed to a 
central affection ; the first of these suggested a process in 
the spinal cord beginning, and at first most intense, above 
the lumbar enlargement ; while the pyrexia, developing 
late in the course of the affection, was evidence of inflam- 
mation rather than of a primary blood state. Had the 
fever been due simply to the cause of the symptom, it 
would have occurred early. Its indication — that there was 
inflammation — agreed with the spinal symptoms. How- 



122 ACUTE ASCENDING MYELITIS. 

ever set up, acute inflammation in the nerve centres always 
tends to more or less irregular and random influence. 
This is no doubt largely determined by the participation of 
the vessels in the process, and by other causes, such as a 
slightly greater intensity in one tract of grey matter in 
which it may spread, or the local influence of a small inflam- 
matory extravasation. Hence inflammation, when set up, 
extends in a more or less random manner, and its symptoms 
are often irregular, at least in some degree. 

The significance of these indications is that, in this patient, 
we had to deal with acute ascending myelitis. This is the 
condition between which and the special " acute ascending 
paralysis " there is generally most difficulty in diagnosis. 
Although the initial excess of the knee-jerk suggests that 
the inflammation began above the lumbar enlargement, and 
that the centres in the latter were merely irritated at that 
stage, yet the complete palsy of the legs shows, however, 
that even then the damage to the cord above the lumbar 
enlargement must have been considerable. As the inflam- 
mation spread, upwards and downwards, the damage to the 
centres in the grey matter of the lumbar enlargement caused 
absolute loss of the knee-jerk, but it would seem that, even 
to the last, the lowest part of the cord on the left side was 
not completely involved, so that a plantar reflex could still 
be obtained. Trophic disturbance, such as the large bulla 
on the side of the heel, does not occur in Landry's paralysis : 
it is an indication of an intensely irritative state of the 
nerves, transmitted to them from the spinal cord through 
the posterior roots. Although the posterior nerve roots 
conduct impressions upwards they transmit nutritional, in- 
fluences downwards. This transmission is, indeed, probably 
by their own nutrition ; the disorder in their molecules 
passes to the tissues in which they end. This bulla, in 
connection with the other symptom, showed that there was 
an intense irritative inflammation in the spinal cord. It 



POSSIBLY LANDRY'S PARALYSIS. 123 

was on the side on which the plantar reflex was abolished — 
that is, on the side on which the inflammation of the grey 
matter, in the lowest part of the cord, was most intense. 
The lad's condition did not allow of our ascertaining exactly 
the state of sensation. 

But, in the lessened movement of the face, of the mas- 
seter, and of the eyeballs, trifling as all were, there was 
evidence that the inflammation was spreading upwards 
into the pons. It seemed to have passed the medulla, ex- 
cept that the heart-sounds were unnaturally short, with a 
peculiar character, seldom met with except in acute dis- 
turbance of innervation, as if the cardiac centre were 
becoming affected. 

I have said that the opinion that he was suffering from 
Landry's paralysis was probably not far from the truth. 
There is no doubt that Landry's paralysis is due to an 
acute blood poison acting on the nerve centres, from below 
upward. All present knowledge leads us to ascribe an 
acute inflammation of similar course to a like cause. 
Both maladies occur under analogous conditions. It is 
probably only a question of a slight degree of difference 
in the nature of the blood poison, whether it simply arrests 
function and causes slight nutritional changes, or whether 
it sets up actual inflammation. Measles may be followed 
by typical Landry's paralysis, without evidence of inflam- 
mation ; and measles may also be followed by an intense 
spreading myelitis. We are learning to see more and more 
distinctly the profound causal influence of toxic blood 
states in producing inflammation of the spinal cord as well 
as of the peripheral nerves, and it is most important to 
recognize the fact that allied blood states seem to cause 
one, or the other, or both. At present, multiple neuritis 
has the hold on professional thought which novelty always 
entails, and central diseases are sometimes overlooked. I 
have lately read some descriptions of acute fatal " multiple 



I2 4 ACUTE ASCENDING MYELITIS. 

neuritis " (without autopsy), due to toxaemia, which I am 
sure were cases of ascending myelitis. 

Among these blood states which act on the nervous sys- 
tem some of the most important are those connected with 
acute specific diseases — the diseases that are due to an 
organismal virus. The question was put to me in this case, 
Was the lad's malady connected with the gonorrhoea? I 
do not know that anything of the kind has been hitherto 
observed as a result of gonorrhoea, but a causal relation 
between the two is highly probable. We know how such 
states are produced by various acute specific diseases ; and 
we know that the poison, the organized poison, of gonor- 
rhoea may induce a subsequent toxemic state which is 
manifested by the arthritis of " gonorrhceal rheumatism." 
Let us consider, for a moment, what this means. 

The organisms of such diseases seem to cause these con- 
sequences, in most instances, by producing a chemical 
organic poison in the blood, and analogy makes it highly 
probable that such an agent is the cause of the arthritis. 
But we know that such products can act on the nervous 
system, peripheral and central, inducing grave disturbance 
of function, and definite, often severe, inflammation ; it is 
therefore not surprising to find that in some individuals, 
especially predisposed, the gonorrhceal virus should cause 
an after-poison capable of producing the terrible effect 
which was seen in this case. Let me remind you of a fact, 
which I may have mentioned before and may have to men- 
tion again, because it is one of the cardinal facts of medical 
knowledge, throwing light on many problems, and, among 
others, on the influence of predispositions. It is the fact 
ascertained by the admirable researches of Dr. Sidney 
Martin on the process by which diphtheritic paralysis is 
produced. He seems to have conclusively proved this, — 
that this paralysis is due to a poison of organic, chemical 
nature; that the poison is not produced directly by the 



INDICATIONS OF SPECIFIC RELATION. 125 

diphtheritic organisms, but that these generate a particular 
chemical substance of the nature of a ferment, which acts 
upon albuminous materials (" albuminoses ") in the body, 
especially in the spleen, and converts them into a poison 
which has this intense action on certain nerve structures. 
It is probable that the mechanism is similar by which 
many other specific organisms give rise to toxic agents. 
You can readily understand that if a person has previously 
been in bad health, as this lad had been, there should be 
some slight defect in the chemical constitution of such 
substances as the albuminoses of the spleen, etc., and a very 
slight defect may render the product of such a ferment 
different from that which would result in perfect previous 
health. A very slight difference in constitution, a little 
more or less of one element, may change atoxic substance 
into a harmless one, and vice versa. Thus we can under- 
stand how it is that the same causal influence shall have 
but little effect in one individual, and shall have a profound 
effect in another, especially in another who has been in 
conspicuously bad health. We can understand, for instance, 
that the organisms of gonorrhoea shall, in one person, give 
rise to a toxic chemical material which acts on the joints, 
and causes the arthritis of " gonorrhceal rheumatism," 
while, in another, the poison produced shall act on the 
spinal cord and set up acute myelitis, as in this case. 

The lad was in a state in which death seemed inevitable. 
In " acute ascending paralysis " (Landry's paralysis), as I 
have said, we have only an arrest of function by the blood 
state ; in inflammation we have also a process of organic 
change, in the vessels and the tissues, which tends to pro- 
gress even apart from its cause. The mere arrest of func- 
tion, once stopped, may not increase, and may be followed 
by steady recovery; but the effects of inflammatory damage 
must persist, and the process itself may continue for a 
time after the blood state which has caused it ceases to act. 



126 ACUTE ASCENDING MYELITIS. 

Hence, I fear that the chances for the poor fellow's life are 
very small. I doubt, indeed, whether he is alive now. 

Although the expectation of saving life may be absent, 
and even the hope of doing so can find no room in reason, 
we are always under the compulsion of striving to achieve 
that which we may not be able to think possible. Our 
knowledge is never certain — even our possibilities may be 
incorrect, and so our hopelessness may be wrong. We must 
act in spite of our anticipations. Therefore, it will be right 
for you to ask, what did I suggest should be done for him ? 

As far as I have been able to see, there are only two 
agents which have any considerable influence upon toxic 
blood states of this kind. One is mercury. I believe the 
influence of mercury in syphilis is only one instance of its 
power over organisms. It is the most striking and perhaps 
the only one surely known to us, but it is probably not 
the only one, and is not likely to be the only one. Some 
years ago, a discovery was made in some researches at the 
Brown Institution which has been almost unnoticed since, — 
that the fatal effects of a certain inoculation (I think with 
the poison of anthrax) could be prevented by mercury. 
Its influence in other diseases of like nature is supported 
by many facts. That on inflammation, which few can 
doubt may be connected with its effect on blood states. 
So I advised that mercury should be rubbed in — a drachm 
of mercurial ointment every four hours. In such a case, 
however, you must "hit right and left;" there is not an 
hour to lose ; you must do anything and everything you 
can, always provided you do no harm. In septicaemia, 
such septicaemia as occurs after childbirth, for instance, the 
agent which has seemed to me effective, and which, as far 
as I could judge, has certainly saved life, is perchloride of 
iron in full doses. So I advised that every three hours 20 
minims of the tincture of perchloride of iron should be 
given. The only other opportunity for treatment, beyond 



FATAL TERMINATION. 127 

ordinary stimulation, was this. He might die from failure 
of the functions of the medulla; they might fail from the 
influence of disturbance of other related parts, or from an 
influence which was not an actual inflammation ; it was 
just possible that if they could be kept active he might tide 
over a period of danger. The measure that has seemed to 
me to have most influence in stimulating and keeping up 
the functions of the medulla, is the hypodermic injection 
of a small quantity of strychnia, one-eightieth of a grain, 
together with a very minute, stimulant dose of morphia, 
about one-thirty-sixth of a grain, repeated every two hours 
if necessary. Of course, if the failure of function were due 
to invasion by inflammation, this could have no effect. 

But there was no reasonable ground for hope that the 
treatment would be effective. The cause is more likely to 
be a chemical substance than organisms, and we have even 
less power over the former than we have over the living 
agents of disease. Had the symptoms been due merely to 
the restraining influence on function exerted by the blood 
state, we could have felt a slender hope that its maximum 
might have been reached. But inflammation, to whatever 
due, is a process with its own effects — proportioned to its 
initial energy, but locally independent of its origin — certain, 
at such a stage, to cause more destruction. Already at the 
limit of the functions essential for life, it could scarcely stay 
there ; the passage of that limit seemed inevitable, and with 
it the thread of life would break. Next week I shall doubt- 
less be able to tell you. 

[In his lecture the following week Dr. Gowers mentioned 
the sequel. The boy lived only six hours. A post-mortem 
examination, made by Dr. Arkle, revealed characteristic 
signs of myelitis, most intense at the place at which the 
inflammation had been supposed to begin — the lower part 
of the dorsal region, just above the lumbar enlargement. 
There, indeed, it had caused the front of the cord to be 



128 ACUTE ASCENDING MYELITIS. 

bulged forward in an unusual manner by the swelling and 
softening of its substance. There was also some softening 
in the mid-dorsal and lower cervical region, where the grey- 
substance was hemorrhagic, almost diffluent. Culture- 
investigation for organisms has been commenced, and the 
pathological results of these and of the microscopical exam- 
ination of the cord, will be published by Dr. Arkle.] 



LECTURE IX. 
LOCOMOTOR ATAXY. 

I. 

Gentlemen : — I desire to-day to direct your attention to 
the disease known as locomotor ataxy. It is a subject with 
which you are all probably more or less familiar, but per- 
haps not so familiar as to make it superfluous for you to 
consider afresh some of its features and some of the lessons 
they convey. The subject is so large that it will be im- 
practicable to bring into the compass of a single lecture all 
the points to which I desire to direct your attention, and, 
therefore, I think it will be wiser for us to devote to it two 
of our weekly meetings. The subject is instructive on 
many accounts. The study of this disease supplies a use- 
ful example of pathological reasoning, and of the mode by 
which we discern the mechanism by which symptoms are 
produced. It is instructive also on account of the wide re- 
lation of its facts : those which you learn in considering it 
have an application to many other definite diseases, and to 
many other general morbid processes. It is also instruc- 
tive because it is a typical example of the class to which it 
belongs, — typical not only in its nature, but typical also in 
its treatment. If you learn these thoroughly you will have 
learned also much relating to other diseases. 

I propose to consider to-day the leading symptom of the 
disease, the ataxy, in reference to its mechanism — to con- 
sider it, not in confusing detail, but with perhaps superflu- 
ous deliberation. It is an advantage in clinical teaching, 



Delivered June 14, 1893. Clinical Journal, September 27, 1893. 
12 129 



130 LOCOMOTOR ATAXY. 

that information can be given in less compressed form than 
is possible in systematic lectures. In the latter, so many 
facts have to be described and discussed in such rapid suc- 
cession, that, in the mind of the student, they are apt to 
jostle one another out of place, so that, at the last, perhaps 
only a very few facts remain prostrate in his mind. I pro- 
pose to avail myself of this freedom, and to strive to fix in 
your mind only the leading facts relating to the subject. 

There are few diseases of which the name has given more 
trouble than that of locomotor ataxy. This name was 
assigned to the malady by Duchenne, with the additional 
epithet " progressive," an epithet which soon came to be 
dropped on account of its clumsiness, and the dropping has 
since been confirmed by the discovery that the adjective 
was inaccurate. The disease in a large number of cases is 
not progressive. The ability to recognise the early stage 
of the disease has revealed to us the fact that at least half 
the cases, I think more than half, are not, or need not be, 
progressive. But the term "locomotor ataxy " is itself some- 
what redundant., because the disorder is one of movement 
in general, and not merely of that which causes change of 
place. So " motor ataxy " would be as accurate as " loco- 
motor ataxy." But the term " ataxy," as a simple term, 
is only applied to disorders of motion, so even the epithet 
" motor " has been largely discarded, and the term 
" ataxy " has been used alone. And yet it has been found 
that even this is inaccurate, because the disease may exist 
in its slighter form without even a trace of inco-ordination. 

Hence the example has been widely followed, which 
was set in Germany, of using a still more general name, a 
term which had been before applied to various affections 
of the spinal cord, the term "wasting of the back," "tabes 
dorsalis." But, again, with the strange swing of the pen- 
dulum which seems inevitable in the progressive altera- 
tion of idea inseparable from the advance of scientific 



QUESTIONABLE NOMENCLATURE. .131 

knowledge, we have found that the disease may exist 
when there is no affection of the spinal cord, and so it has 
been necessary to supplement the term " tabes dorsalis " 
with the term " peripheral neuro-tabes." I shall explain 
the necessity later on. It is rather surprising that in this 
difficulty more writers have not been disposed to fall back 
upon the name which has sometimes been applied to this 
disease, that of DncJicnne 's disease. The labours of that 
most distinguished and most energetic clinical investigator 
of diseases of the nervous system have been recognised by 
the ascription to him of the ownership of three maladies, 
— two diseases and one paralysis, — pseudo-hypertrophic 
paralysis, and locomotor ataxy are Duchenne's " diseases," 
and labio-glosso-laryngeal palsy is Duchenne's "paralysis." 
But this method of nomenclature has its disadvantages. 
It involves a grave burden upon the memory of the 
student, especially when it is applied to diseases and 
symptoms. 

It has not only inconveniences ; occasionally, in the 
admiration of one man, an injustice is done to others. I 
yield to no one in my admiration for Duchenne. Duch- 
enne's description of the disease first called general atten- 
tion to it, and the name he gave it was adopted. But 
what constitutes the discovery of a disease ? If to dis- 
tinguish the symptoms from those of other similar 
maladies, to affirm from physiological considerations that 
a definite structure in the nervous system is diseased in 
such cases, and that this disease is the cause of the symp- 
toms, and then, in the body of a patient, to find and 
demonstrate that very structure to be diseased, — if this 
is not the discovery of the disease, I would ask you, 
gentlemen, what is. And that was done for locomotor 
ataxy by an English physician at King's College Hospital, 
Dr. Todd, and done nearly 15 years before Duchenne's 
description of the disease was published, and probably 



132 LOCOMOTOR ATAXY. 

many years before he had begun to suspect its special 
character. If locomotor ataxy is to be called by the name 
of any physician it ought to be called " Todd's disease." 

Let me now direct your attention to the general feat- 
ures of the cases that I have to show you, and then 
proceed to consider the leading symptom of the disease, 
its origin, and nature ; next week we will consider in de- 
tail some of the other symptoms, and some of the general 
practical questions connected with the affection. 

The first patient is a man aged 41. He can tell us of 
no apparent cause for the disease. But most of you 
know that there is one antecedent that must always be 
searched for — syphilis. His preceding history, however, 
affords no evidence of this disease. But those of you 
who were here a few weeks ago will remember that I in- 
sisted on the fact that the absence of a history of syphilis 
does not enable us to exclude the disease unless we can 
exclude the conditions of its causation. I need not re- 
peat the considerations which compel this conclusion. 
We are not able to exclude it here. Three years ago he 
began to suffer from tightness and numbness around the 
chest across the front, with some pain there. These symp- 
toms in the chest were followed by numbness in the feet, 
a year and a half ago, and then by shooting pains in 
the thighs, extending to the calves, heels, and arms, and 
accompanied by some unsteadiness in walking in the dark. 
He says also that some weakness of the legs came on ; 
but patients with this disease very often describe weakness 
of the legs when there is none. They mistake the diffi- 
culty of co-ordination for deficiency of power. 

Tardiness of micturition also developed, a symptom 
which is sometimes the earliest to attract the attention of 
the patient. Remember that many sufferers from diseases 
of the spinal cord first seek medical advice on account of 
difficulty of micturition ; unless we are aware of the fact, 



ILLUSTRATIVE CASES. 133 

they may be treated for a long time, and treated unsuc- 
cessfully, because the real cause is not suspected. 

There was also transient double vision, — another early 
symptom of the disease, the relations of which we shall 
have to consider next week in greater detail. 

He has now, as you see, slight inco-ordination of the 
left hand and of the legs, greater in the left leg than 
in the right. When told to touch his nose with his fore- 
finger, he succeeds fairly well. With the left hand he 
can unbutton and button his waistcoat. If made to hold 
both his hands out, when his eyes are shut, there is 
very little spontaneous movement to be detected. When 
made to walk without the aid of his stick his gait is a little 
uncertain. When he puts his feet close together and shuts 
his eyes, you observe that he has difficulty in maintaining 
his balance. When asked to put his feet close together 
with his eyes open, he is just able to stand upright, not so 
steadily as is natural, and if then he raises his head up the 
tendency to sway is distinctly greater. In this position the 
base of support of the body is reduced in area, the muscu- 
lar contractions have to be more accurately adjusted to 
maintain equilibrium, and the defect in the power of adjust- 
ment reveals itself. When, after placing my hand in a 
certain position, I ask him, with shut eyes, to touch it with 
his left foot, very little inco-ordination is revealed. His 
defect shows itself chiefly in walking and in standing. 
There is no knee-jerk in either leg. A little impairment 
of sensibility to touch can be found, chiefly on the outer 
surface of the legs. Reflex action from the skin is defec- 
tive, and the reaction of the pupils to light is slight. 

In the second patient, the gait is much more defective 
than in the first. His toes are raised too high as he walks. 
When asked to stand still with his feet w T ide apart he can 
do so, but with the feet close together he has great diffi- 
culty in standing. He separates his feet to increase the 



154 LOCOMOTOR ATAXY. 

base of support ; but even then the muscles are in constant 
action, so that the toes are every moment raised, because 
the over-action of one set of muscles is so great that it has 
to be compensated for by the contraction of another set, 
and this is also too great. Withdraw his visual guidance 
and he is quite unable to stand. After observing the posi- 
tion of my hand he cannot touch it with his left foot while 
his eyes are shut. His foot goes too much to the left. 
With the right foot he does better, but this also goes too 
high. He succeeds in touching his nose with the tip of his 
forefinger while his eyes are shut. When made to hold 
out both hands with his fingers extended, involuntary move- 
ments are seen, the action of the muscles which should 
keep the limbs at rest being disordered, like that of the 
muscles during movement. In this patient also there is no 
knee-jerk in either leg. 

The symptoms in this case are of six years' duration ; 
and the unsteadiness has been considerable, and accom- 
panied by shooting pains for five years. For three years 
he has had symptoms of unusual character in certain cra- 
nial nerves which also we shall consider next week. The 
muscles of mastication are affected. He has difficulty in 
approximating his lips and likewise some paralysis of the 
ocular muscles. In addition, he has deficient reflex action 
in the pupils, impairment of sensation in the limbs, and 
also in the face. 

In the other patient we could only recognise syphilis as 
a possible antecedent; in this, it is certain. We have dis- 
tinct evidence of its occurrence. Twelve years ago he had 
the primary lesion, followed by sore throat. 

These, then, gentlemen, are the chief features of the 
disease. We will now consider especially the characters 
of the leading symptom, that round which the others are 
grouped, as it were about a centre, and which, although 
not invariable, is vet the dominant element in the devel- 



ixco-ordixat: 

::t: : -^ ; t In ab :ase= ever. vbier :b:= symarmm zzts 
net exis: mr.LLim ran be :ra:ea vLaiLv are :ar_abie abb- 
mately, of producing it. 

7be ."-'- :■: .: ::..:::: ataxy v = vvy:::m 

which, as its name expresses, is in aspect a motor symp- 
tom. But it is not a motor symptom in its nature. It is 
r :: zee :: a zrimary ae ran verier.: : :' r::::: rr: :essea are 
motor structures. In a typical case, if you test the strength 
of the limb in which there is the greatest disorder of move- 
ment, you find no deficiency of power, and if you examine 
:: y: j vva r. : :ra:e ::' v.vvv v:.::: M: reiver : y : 
= :r_: are wbv vie rvvmsmre vie rr. :::■: =:r em.arei :be 
i : rrex n'rbe brair. Lie bares via: v ;; v i :he ivir.ia 
:be :eb = if :be aaieriir mrrvzz :f Lie :ir: Lie vires 
vv-: raas vrriayb vie ar.rer::: rer eriirs:: bze nemes 
ar. a ever, r. .:: r v iys in be ma = Le = y: fr.a r. : :ra:e ::' 
- 7 be viiii r sir z::z re= : v i y vv b 

it very different when you examine the sensory structures. 
Li ib : a ~ e 5 vi " b vi vie srbrai ::ra b zb"e::ea — v:i b bvey 
:::i5Vii:e :be yrea: maLrivy — -.ve vv: Lbease vv Lie :-. ;- 
■swrp part of the cord. Wherever there is inco-ordination 
there is sclerosis in the posterior columns at the place at 
which the posterior nerve roots from the seat of the inco- 
irviLiv zzv- in:: vie ::::". zrz zi=: zeyererzLir :: :be 
ivvr.v nerve r: ::= Tie ex = :er:e b:.v zbezse vbzere 
Lee r irieriir vev.e r: i:s enter Lie ::rz ana ::" zeveverzbir 
in :ne :::: ; viewer .es i ryev Lva: bze esservbai ieLir 
ar.ae.Lyiry vie rvvvv if an in:errvr:i:n in. :be : : v: i ::- 
iry :"::.::. : v ::' :be yisreriir nerve n :r= Ave :ba: :::.- 
elusion is remarkably confirmed by some rare cases in 
which the posterior nerve roots have been damaged 05^ 
other causes. In one case especially (recorded by Dr. 
H j~be= Lev rev in vv:b vie r. aven: baa v: vv ve ram : zrs 
ariv many ::' ve river:: :::v Lvere v.-ere Lie vyvirni 
symptoms of locomotor ataxy. This case ye a: 



136 LOCOMOTOR ATAXY. 

importance ; it establishes the fact that the symptoms of 
the malady we are considering may depend on a simple 
lesion. It affords us one of the firm facts of pathology by 
which we may ascertain the meaning of other complex 
phenomena. 

But the disease of the root-fibres is not the only lesion 
in tabes. All the way up the cord, above the place at 
which the root-fibres entering the cord are conspicuously 
diseased, we find degeneration of the posterior median 
columns — of that part of these columns that is adjacent to 
the posterior median septum, — the so-called " column of 
Goll." At the lumbar region, where, as a rule, the root- 
fibres are affected, this degeneration of the posterior median 
columns widens out, so as to blend with that at the en- 
trance of the nerve roots. That is because the fibres which 
ascend in the median columns reach these from the roots 
by passing through the external parts of the posterior 
columns. It is because the median parts are composed of 
root-fibres that pass to them without interruption, and 
ascend in them without decussation. Hence disease of the 
lumbar roots necessarily entails the degeneration of the 
median columns, and its extension outwards to the root 
region of the affected fibres. The fibres degenerate up- 
wards, and do so in the same way if the lumbar roots are 
destroyed by any other morbid process. It is thus certain 
some root-fibres ascend the cord without interruption, and 
that these fibres are diseased in tabes. That is the first 
great pathological fact for you to remember. 

Now, leaving this point for the present, what evidence 
can we discern as to the way in which disease of the nerve 
roots causes the symptoms of this malady ? Certain clini- 
cal facts, when taken together, have a very clear pathologi- 
cal significance. First, the leading symptom, ataxy, exists, 
in its typical form, and even in high degree, in many cases 
in which there is no impairment of any form of cutaneous 



AFFERENT IMPULSES BY COMPRESSION. 137 

sensation. Further, in agreement with this, we have the 
fact that when there is impairment of cutaneous sensation 
there is no proportion between it and the amount of inco- 
ordination. It is, therefore, certain that the disease of the 
posterior nerve roots does not cause ataxy by interrupting 
the impressions conveyed from the skin. Yet it is also 
certain that the symptom is due to the interruption of some 
impulses which these roots convey. 

What other afferent impulses pass to the cord by these 
roots ? They are the impulses from the deeper structures, 
from the muscles especially, also from the fibrous struc- 
tures, from the fasciae, perhaps from the tendons, and cer- 
tainly from the joints. Remember that we must not con- 
found afferent impulses and sensory impressions. It is 
probable that the afferent nerves are continually being tra- 
versed by impulses which do not act directly on conscious- 
ness, and do not, when in normal degree, produce a true 
sensation. We are unconscious of any sensations in our 
muscles at the present moment. But a vigorous compres- 
sion of any muscle will at once convince you that afferent 
impulses can be readily generated in it ; so also will an 
attack of nocturnal cramp, and so also will the process of 
going upstairs on the following morning. In cramp of the 
calf, the afferent nerve-fibres within the muscles seem to be 
stimulated by their compression in consequence of the nar- 
rowing and widening of the strongly contracted muscular 
fibres, and when the nerves are rendered hyperaesthetic by 
that disturbance, they are stimulated in a very marked de- 
gree by the tension to which they are exposed when the 
muscle is extended in mounting stairs. ... So that 
we have evidence that afferent impulses are generated in 
these fibres by compression during contraction, and by 
tension during the passive elongation which the muscles 
endure on every movement. We can understand these 
facts by the mode in which these afferent fibres arise in the 



138 LOCOMOTOR ATAXY. 

muscles. According to the investigations of Tschiriew, 
they commence in the interstitial tissue between the fibres, 
and must thus be equally exposed to the mechanical effect 
of compression or of tension. Thus, by the exclusion of 
cutaneous impulses we are driven to refer the origin of 
ataxy to the interruption of these deeper impulses. We 
can perceive more of the features of the impulses from the 
muscles, than of those from other deep structures, and the 
large extent of the muscular tissue makes its probable that 
they constitute the chief part of the deeper impulses. 
Moreover, the phenomenon of muscular co-ordination sug- 
gests that they, rather than the impulses from the joints, 
etc., take the chief parts in its regulation. This is con- 
firmed by the constancy with which the knee-jerk is lost in 
locomotor ataxy. Whatever is the precise mechanism of 
the knee-jerk, it certainly depends upon a reflex process in 
which the afferent impressions proceed either from fibrous 
tissues or from muscles, and probably chiefly or exclusively 
from the muscles. But the constancy of that loss confirms 
the conclusion that it is by the interruption of these afferent 
muscular impulses that the ataxy is produced. 

What is the significance of the degeneration in the pos- 
terior median column ? We find it whenever the posterior 
nerve roots are destroyed. Moreover, if the nerve roots 
are destroyed on one side only, the degeneration of the 
posterior median column is on that side ; this and the facts 
already mentioned show, as I have stated, that nerve-fibres 
pass from the posterior root, through the posterior column, 
into the posterior median column on their own side, and 
do not cross. And as this degeneration of the posterior 
median column is constant in locomotor ataxy, we cannot 
doubt that the fibres which constitute it are some of those 
the disease of which gives rise to the symptom in question. 
And that is confirmed by two other very interesting facts. 
If that posterior median column is divided on one side in a 



MECHANISM OF CO-ORDINATION. 139 

unilateral lesion of the cord, the effect is to cause inco- 
ordination in the muscles of the same side; whereas it is 
found that an extensive unilateral lesion causes loss of pain 
and sensibility on the opposite side. Further, in advanced 
tabes we commonly have a very marked loss of the muscular 
sensibility : the muscles may even be insensible to pressure 
or extension, thus confirming the conclusion that there is 
disease of their nerves, and supporting the opinion that 
this is the lesion which causes the characteristic ataxy of 
developed tabes. 

Where do these posterior median fibres go ? You must 
often have been struck by the similarity between the mode 
of standing and walking in some cases of ataxy, in which 
the power of maintaining equilibrium is especially de- 
ranged, and that of a patient with cerebellar disease. 
These posterior median fibres go up to the posterior 
median nucleus of the medulla; and it has been proved 
that there are many other fibres proceeding from the cells 
of that nucleus to the middle lobe of the cerebellum, the 
part of the cerebellum that is alone concerned in co- 
ordination. The probability is thus very great that these 
fibres conduct impulses which reach the middle lobe of 
the cerebellum and guide it in its co-ordinating function. 
So that we seem to perceive two processes in the mechan- 
ism of co-ordination : (1) Impulses from the muscles go to 
the cord; some of these must enter the grey matter to 
subserve the reflex action on which the knee-jerk depends, 
and they probably regulate a series of subsidiary co-ordinat- 
ing mechanisms. When you stand, you stand by a volun- 
tary impulse, but it is probable that the voluntary impulse 
acts through a mechanism in the cord which determines 
the arrangement of the movements for standing. The 
action of this mechanism is conspicuously seen in cases in 
which disease at the middle of the cord cuts off the lower 
part. Then, as you well know, spastic paraplegia is pro- 



Ho LOCOMOTOR ATAXY. 

duced, and the extensor spasm perfectly reproduces the 
condition of the limb in standing. That extensor spasm, 
which is attended by a gradually increased knee-jerk, is 
apparently dependent upon arrangements which are acted 
on by these impulses from the muscles. (2) Impulses pass 
up the cord, and probably reach the cerebellum, and 
through the cerebellum they may act on the motor cerebral 
cortex, and influence the relative energy of its cells. Thus 
we have this double reflex process of co-ordination from the 
muscular impulses, one by the cord, the other through the 
cerebellum. When a sensation of pain is produced in a 
muscle by a strong impression on its nerves, it is probably 
through those that terminate in the cord ; but we have no 
direct proof of this, and it has no special concern for us in 
our present problem. We perceive, then, that muscular 
inco-ordination is due to loss of impulses from the deeper 
structures, chiefly from the muscles. If there is a total 
loss of all the impulses, the muscle reflex is abolished, the 
knee-jerk is lost, and we have extreme ataxy. If there is 
only a loss of the impulses that pass up to the cerebellum, 
when there is disease of the posterior column above the 
lumbar enlargement (as in ataxic paraplegia), the knee- 
jerk is not lost, and we have only a moderate degree of 
inco-ordination, manifested especially in the defective main- 
tenance of equilibrium, and almost identical with that of 
cerebellar disease. 

I mentioned, just now, that the spinal cord is not invari- 
ably affected in tabes. Exceptions to the common rule are 
extremely rare, but their occurrence is well established. 
When the cord is free from disease the peripheral nerves 
have been found to be degenerated. They suffer, indeed, 
in a large proportion of the cases in which there is degen- 
eration of the root-fibres ; the peripheral endings are 
altered in chief degree. In the cases in which the cord is 
unchanged this lesion of the nerves, usually concurrent, is 



THEORETICAL PROBLEMS. 141 

isolated, and the sole cause of the symptoms. These do 
not differ from the symptoms of cases with the usual lesion. 
Hence, we are justified in concluding that the nerve-fibres, 
the disease of which gives rise to the characteristic symp- 
tom, ataxy, are the same in both forms. The nerves which 
are affected first and most in these cases, as in the others, 
are the nerves of the muscles. So that, whether we have 
disease of these muscle nerve-fibres in the posterior nerve 
roots and posterior columns of the cord, or disease in their 
peripheral extremities, we have precisely the same condi- 
tion ; if the mechanism is the interruption of the conduct- 
ing fibres, the effect must be the same, wherever in their 
course the lesion is situated. Hence, in " peripheral 
neuro-tabes," as the rare form is termed, — locomotor ataxy 
without disease of the cord, — we have a condition precisely 
similar to that which depends on the spinal lesion. Hence, 
also, there is ataxy similar in its features in the other forms 
of degeneration of the peripheral nerves, such as are pro- 
duced by Alcohol and by Arsenic. It may even be im- 
possible, from the symptoms themselves, as far as the 
ataxy is concerned, to distinguish a case of true locomotor 
ataxy from one of what is called " alcoholic pseudo-tabes." 
I hoped to have gone over to-day other points regarding 
the nature of the lesion, but it will be better to postpone 
these until next week. I must be content to-day if I have 
succeeded in giving you a clear conception of the me- 
chanism of the special symptom of the disease, or at least 
of the more salient elements of the evidence regarding its 
nature. I would only point out to you, in conclusion, how 
interesting is the enlargement of our ideas regarding this 
disease which has come from modern research. There is 
much that we cannot understand concerning the precise 
mechanism of co-ordination and of its defect; nevertheless, 
we have a glimpse into the process, though we cannot 
surely perceive all its outlines. It is certain that the 



142 LOCOMOTOR ATAXY. 

afferent nerves of muscle are stimulated by the changes 
which they must endure in the two states of the muscle ; 
the muscular contraction when the muscle is active, and 
the tension it undergoes when its opponent is acting, alike 
generate afferent impulses. These we do not ordinarily 
perceive, except in the vaguest manner. They are doubt- 
less concerned in the production of our conceptions of 
posture and movement, but we only perceive them as sen- 
sations, when from some cause they become excessive. 
But the}- must be constant, in unperceived degree, influ- 
encing and guiding the central mechanism. 

Consider the subject over at your leisure, and I think it 
will become clear to you, and that you will find assistance 
from it in understanding many processes and many prob- 
lems to which I have not ventured to refer. 



LECTURE X. 
LOCOMOTOR ATAXY. 

II. 

You may remember, gentlemen, that last week we 
studied at considerable length the chief symptom of loco- 
motor ataxy and its mechanism. To-day we will briefly 
review the other symptoms of the disease. They are, how- 
ever, so numerous that I shall have to content myself with 
a mere glance at those that are of chief importance and at 
their relations, considering in more detail some that are 
illustrated by the cases we examined, or that are of most 
significance, or with which you are not likely to have become 
familiar. 

The morbid process which, as you saw in the microscopi- 
cal sections, is indicated by an overgrowth of the connective 
tissue, is essentially a degeneration of the nerve elements, 
beginning in them. Such degeneration has many causes. 
It seems sometimes to be the result of a mere inherent de- 
fect of vitality ; sometimes it is a local manifestation of 
senility; sometimes it is due to the influence of general 
conditions, depressing emotion, and like influences ; but in 
the vast majority of cases it is the result of the action on 
the nerve elements of a toxic agent. We see it as the effect of 
chemical agents of inorganic nature, and also as the effect 
of certain organic chemical agents which are produced by 
minute organisms — such, for instance, as alcohol, which is 
due to the growth of minute organisms outside the body, 
and materials of unknown composition produced by the 

Delivered June 21, 1S93. Clinical Journal, October, 1S93. 
143 



144 LOCOMOTOR ATAXY. 

minute organisms which constitute the virus of some acute 
diseases. Such organisms cause their own direct effects, 
but they also leave behind them in many cases such a sub- 
stance as I have referred to, which acts upon nerve elements 
as inorganic poisons may do, and causes degeneration. 
And this, which has been proved to be true of the virus of 
some acute specific diseases, seems also to be true of the 
chronic specific disease which is so frequent an antecedent 
of ataxy, syphilis. This was, you will remember, certainly 
traceable in one, and possibly in the other, of the patients 
whom we saw last week, and whom we will presently again 
examine. As a fact, this antecedent is to be ascertained in 
more than two-thirds of the cases ; and it has probably 
preceded tabes in at least four-fifths. Such a relation 
means a causal influence in the majority, for mere coinci- 
dence will explain only a small proportion. At first the 
statement of these facts was received with general scepti- 
cism. But we have to be careful, in science, how we deny. 
Some denied the possibility of the causal relation, but they 
have had to reconsider their denial ; fresh observation of 
facts yielded evidence of overwhelming cogency. One rea- 
son why the relation was doubted was because it was found 
that anti-syphilitic remedies did no good to the disease; 
and the fact is unquestionable. But the mystery is ex- 
plained when we perceive that only on the lesions which 
are the direct result of the syphilitic organisms does anti- 
syphilitic treatment exert its influence ; on those lesions 
which are the result of the toxic material produced by the 
organisms, the anti-syphilitic treatment has no influence. 
This material has not been isolated, but the analogous 
material has been isolated in some acute diseases dependent 
upon organisms ; and so close an analogy can be traced 
between the whole series of such diseases which have after 
effects, that we may feel reasonably sure that it is in this 
way that syphilis produces the disorder we are now con- 



OPERATIVE EXPERIMENTS. 145 

sidering. It is not possible for me now to describe to you 
the evidence, but it is, in my opinion, convincing. In these 
facts we have the secret of the inutility of anti-syphilitic 
treatment in cases of locomotor ataxy, in which the disease 
is, nevertheless, the sequel of syphilis. 

You will remember that we traced the chief symptom of 
tabes, the ataxy, simply to the interruption of the muscle 
nerves and the arrest of the afferent impulses which guide 
alike the spinal and the cerebral motor centres. You will 
also remember that I pointed out to you that, in this mechan- 
ism, it makes no difference in what part of the nerve fibres 
the interruption takes place, and that when the ends of the 
nerves alone are diseased, the effect is the same as when 
the same fibres are diseased in the nerve roots or within 
the cord. 

A curious historical fact may be mentioned in this con- 
nection. In what may be termed " medical surgery," from 
time to time, some operative procedure becomes fashionable ; 
it is adopted on all sides, partly on the strength of an in- 
itial laudation, and partly because it is something to " do " 
where little had been effected. After a time, if it possesses 
no real value, it sinks into desuetude. Of late we have 
had an epidemic of " suspension " for this malady. A little 
before, it was nerve stretching which was said to do remark- 
able good in cases of tabes. The curious fact to which I 
allude is this, that the first patient who seemed to derive 
benefit from nerve stretching was about to undergo the pro- 
cedure a second time, but died under the anaesthetic before 
the operation could be performed, and so afforded patholo- 
gists an opportunity of correlating the operation and the 
morbid process. The operation, unfortunately, was only 
partially utilised. It was found that there was no discerni- 
ble disease of the spinal cord or of the nerve roots. The 
peripheral nerves were not, in that case, examined ; they 
have been examined in others and found diseased in so 



146 LOCOMOTOR ATAXY. 

many, that there can be little doubt that the case I have 
just referred to was one in which the degeneration was at 
the periphery of the nerves. I mention this fact to impress 
on your minds the occurrence of this peripheral change. 
It has been found to be exceeding common, if not constant, 
in tabes, although it is very rarely confined to this position. 
If it is the only lesion, there is no disease in the posterior 
roots. The disease above the ganglia seems to be an inde- 
pendent, coincident, degeneration in the same fibres. 

The disease is not limited, however, to the afferent mus- 
cle nerves (to which I especially directed your attention 
last week), although their affection seems to be the primary 
and essential element. The nerves from the skin suffer in 
a large proportion of the cases, and, in consequence, loss 
of sensation to touch and to pain and to heat (usually to 
some, occasionally to all) is very common, and is distribu- 
ted according to the position of the nerve lesions. The 
anaesthesia, like the ataxy, may be due to disease either of 
the nerve roots in the cord or in the periphery. It is found 
sometimes in the arms, and there is, occasionally, a similar 
loss in the cutaneous sensibility of the head. We may 
have anaesthesia in the region of the fifth nerve ; and de- 
generation of the optic nerve, as you know, is not rare. 
The latter is a typical nerve degeneration, involving the 
peripheral part of the nerve, and is a visible type, in a nerve 
of special sense, of that which occurs in the sensory nerves 
of the limbs. 

The process of degeneration is one of molecular change. 
But the function of the sensory nerves is carried on by 
molecular change. It is thus that they perform their mar- 
vellous function of transforming, for instance, the mechani- 
cal force of motion, in a touch, into nerve energy, or the 
thermic force, which is another form of motion, into nerve 
energy. And the molecular changes of degeneration seem 
to give rise to nerve impulses similar to those which are 



A -i: : V MALADY. 147 

produced under normal circumstances, — similar, I mean, 
as regards their general character, not as regards their 
special occurrence. Hence we have the symptom, so famil- 
iar to you, of the pains of tabes. Most common are the 
peculiar, sudden, sharp, " lightning " pains ; but duller 
pains are very common ; and they are often curiously 
" rheumatic" in character, so that they are almost always 
at first mistaken for rheumatism. So, indeed, with less 
excuse, are the sharp momentary pains. This mistake is 
facilitated by the fact that change in weather, especially 
change to cold, has a remarkable effect in increasing these 
pains, just as it does the pains of true rheumatism, and 
many patients have been treated for several years as the 
subjects of rheumatism or of gout, whose pains were the 
result of this malady. These are felt most often in the 
legs, but also sometimes in the trunk and sometimes in the 
arms, and occasionally with great severity even in the head. 
In the head and trunk they are apt to be mistaken for sim- 
ple neuralgia, and even thought to be the indication of 
encephalic or abdominal disea e 

Thus, these being the essential symptoms of the dise- ise 
it is by its nature a sensory malady; it is an affection of 
the sensory structures. Its dominant feature, the inco- 
ordination, is, as I told you, motor only in aspect. The 
cardinal symptoms of the disease are the result of changes 
in afferent paths. They are, however, often associated 
with subordinate symptoms which are actually motor. All 
toxic agents which may act, primarily and chiefly, on sen- 
sory structures, can also act, to some extent, on motor 
structures, and some of the agents often act on these in a 
preponderant degree. 

Among the motor structures which are most often 
impaired in tabes are the nervous structures for the 
bladder, sometimes those of the sphincter, but more com- 
monly those of the wall of the bladder. The wall of the 



148 LOCOMOTOR ATAXY. 

bowel may suffer also and give rise to constipation ; this is 
inconvenient, but the weakening of the wall of the bladder 
involves definite danger. In consequence, the bladder is 
not emptied ; there is residual urine, and that which 
descends from the kidneys overfills the bladder ; the con- 
stant overfilling necessarily weakens still more the wall, 
because when overdistended its muscular power is rela- 
tively more incompetent, and it is less and less able effici- 
ently to contract. Chemical changes occur in the residual 
urine, and cystitis is excited, with a secretion that increases 
the alteration. The increased pressure in the bladder, thus 
gradually augmented, acts back on the kidneys, interferes 
with their function, and ultimately induces disease in them 
of the nature familiar to you as surgical kidney. The 
blood, from the first, is not properly relieved of effete 
material, which seems to become, at last, actually toxic, 
and a state of imminent peril to life is often thus induced. 
Of all this chain of effects the patient may be unaware. 
The overfilled bladder indeed often overflows, and incon- 
tinence reveals the condition. 

But overflow does not always occur, or occurs so sel- 
dom as to attract little notice, and lowered sensitiveness 
may aid in preventing any consciousness of what is wrong. 
Remember that you must never take a patient's statement 
as true that he empties the bladder. Patients are con- 
stantly under the impression that the bladder is emptied, 
when you may easily ascertain by percussion over the 
pubes that a considerable amount of urine remains in the 
bladder after micturition. This evil may reach a high 
degree in a patient who is in the early stage of the disease. 
It is the chief way in which locomotor ataxy causes death; 
and death in this way can always be prevented. When- 
ever you suspect residual urine, ascertain whether your 
suspicion is correct by passing a catheter. Remember that 
it is absolutely essential for the bladder to be perfectly 



EFFECTS ON THE URINARY SYSTEM. 149 

emptied at least once a day; and if there is any decompo- 
sition of the urine or distinct muco-pus in it, the bladder 
must be daily washed out with a disinfectant. The effects 
of the retention on the kidneys and their function when 
the patient has been brought to the edge of disaster, are 
sometimes precipitated by the reflex effect of the passage 
of a catheter; then the patient is said to have "catheter 
fever," but the condition would have developed spontane- 
ously in a few days, and is due essentially to want of the 
previous use of the instrument. Only two days ago I saw 
a gentleman whom I saw also a year ago in the early stage 
of this disorder. At that time he was having mysterious 
attacks every few weeks, in which considerable pyrexia 
lasted for several days. The doctor who was attending 
him had been greatly puzzled by these, and suggested 
various theories to explain them ; but I found the patient 
was not emptying his bladder. Such attacks of pyrexia 
in that association are generally due to the interference 
with the action of the kidneys and the effect on the blood. 
The patient commenced the use of the catheter, had one 
more slight attack of pyrexia, had since used the catheter 
every day for a whole year, and had not had another 
attack. 

I ought to add, to avoid misconception, that incon- 
tinence is not always due to overdistension, any more than 
overdistension always causes incontinence. In many 
diseases of the spinal cord you have paralysis of the 
sphincter, urine is always escaping, and the bladder is 
always almost empty. In some others, the bladder is peri- 
odically emptied perfectly, by a pure, involuntary, reflex, 
or automatic process. But in locomotor ataxy incon- 
tinence is generally due to overfilling. 

Of other motor symptoms, the next in importance are 
those with which we meet in the eye, of which the most 
common is the loss of the reflex action of the iris to light. 



ISO LOCOMOTOR ATAXY. 

This seems to be due to changes in the centre for this 
movement in the nucleus of the third nerve. Instead of 
this loss, or with it, there may be loss of accommodation, 
or loss of the action of the iris associated with accommo- 
dation. Frequently there is weakness of external ocular 
muscles, sometimes amounting to complete paralysis. 
Such weakness is usually at first transient, but after several 
successive attacks, which last longer and longer, the loss 
of power finally becomes persistent, and it may be present 
in muscles of both sides. All these ocular symptoms 
are probably due to central degeneration in the related 
nuclei. 

There is one important fact connected with this loss of 
action of the pupil to light. It is exceedingly common in 
tabes ; tabes generally has syphilis for its antecedent, and 
this is also true of the isolated loss of reflex action to 
light, apart from the other symptoms of tabes, or even 
from any symptoms of disease of the nervous system. 
Whenever you meet with it as a persistent, isolated symp- 
tom, you will always be justified in suspecting that the 
patient has had syphilis, and in most all cases you will find 
the suspicion verified. This indication is often of very 
great importance as putting you on the track of syphilis 
when you would not otherwise suspect it. 

Other cranial nerves rarely suffer in tabes ; but in one 
of the patients I show you, by the courtesy of my friend, 
Dr. J. Taylor, under whose care the man is, there is a 
remarkable affection of the motor cranial nerves ; not 
only the eyeball muscles, but the muscles of mastication 
are weakened, while the face, palate, and larynx are also 
all more or less paralysed, one vocal cord being 
motionless. 

Remember this case as an example of the wide extent 
of cranial nerve-palsy we sometimes meet with. 

There may be some actual loss of power in the limbs, 



EFFECTS ON NUTRITION OF TISSUES. 151 

but only in late cases of true tabes. It is due to the fact 
that, ultimately, even the spinal motor structures may 
occasionally suffer ; but such weakness is not part of the 
malady in its common form. 

Allied to the pains (which, I should have added, are 
often curiously paroxysmal) we have other paroxysmal 
symptoms which I need only mention — those which are 
called " visceral crises " — gastric pain and vomiting, laryn- 
geal spasm, nephritic pains, rectal pains. These I can 
only mention to-day. But the affection of the sensory 
nerves has often another and very important consequence. 
The sensory fibres of the posterior roots are those which 
govern nutrition in all the structures except the muscles. 
We do not know how they govern nutrition ; indeed we 
can only say that their own nutritional state seems to 
determine that of the tissues, so that the latter is dis- 
ordered when the nerves are actively diseased. If they 
are the seat of acute inflammation, such as may be pro- 
duced by passing a thread with some irritating material 
through the nerve, we have acute changes in the skin, but 
when there is merely chronic disease, slow, and without 
irritation, we have only a gradual thinning of the skin and 
wasting of the bones. For instance, such disease of the 
nerves of the arm gives rise, in the finger-tips, to thinning 
of the skin, and distinct narrowing of the ends of the 
phalangeal bones, and often also changes in the joints, by 
which adhesions form. When you have a peculiar irrita- 
tion of the nerves, such as gives rise to the severe pains 
of tabes, changes may occur in the nutrition of the skin. 
The irritation of the nerves is shown by the intense hyper- 
esthesia that developes at any spot in the skin to which 
the pains are referred. The influence on nutrition was 
curiously shown by one patient who had such localized 
tabetic pains in various spots on the hairy scalp. After 
the pains had lasted for a (qw days every hair broke off 



152 LOCOMOTOR ATAXY. 

near its root, and when the pains ceased, the growth of the 
hairs became natural. Among the most common trophic 
changes, however, are those of the bones and joints, when, 
instead of wasting, as they sometimes do, they enlarge, 
and new bone forms in an irregular manner. This may be 
due to an irritation, rather than to a mere defect of nerve 
influence. Its occurrence is an interesting illustration of 
the degree and extent in which the deeper nerves suffer in 
this disease. 

One other trophic disturbance is both common and of 
great practical importance. It is the tendency to deep 
"perforating ulceration" on the toes, consequent on slight 
injury. It may reach the bone and lead to necrosis. 
These ulcers are often set up by the deep cutting of a corn. 
Always impress upon a tabetic patient that no corn should 
ever be cut ; it may be softened by an alkali, and rubbed 
with sand-paper, but should never be cut. 

The symptoms of tabes are thus, you see, numerous and 
varied ; and according to their grouping they present very 
different aspects. If you remember the leading features 
you will seldom have any difficulty in arriving at a diag- 
nosis. But there are certain special sources of error in 
diagnosis which it may be well briefly to point out to you. 
I cannot attempt even to glance at all the elements of the 
diagnostic problems presented by the disease, and must 
limit myself to a few which are either of special importance, 
are instructive, or are likely to escape your notice until the 
occasion arises for using the absent knowledge. In patients 
who are in the first stage of the disease, before ataxy has 
developed, and in many of whom it never does develop, 
uncertainty is sometimes caused by the limitation of the 
chief disease to the dorsal region. The pains are then felt 
in the trunk, and may be thought, and often are thought, 
to be due simply to intercostal neuralgia. But loss of sen- 
sation accompanies them ; and if you examine the legs 



DIFFICULTIES OF DIAGNOSIS. 153 

carefully you will always find the knee jerk absent, even 
when there is no anaesthesia of the limbs, and no pains are 
referred to them. Such a state has also been mistaken for 
growth in the spinal bones, but in this, the terrible pain is 
especially related to movement of the spine, and that rela- 
tion is never present in tabes. 

Other difficulties in the recognition of the malady may 
be due to the unusual character of the symptoms, or to the 
preponderance of special symptoms which may bring the 
patient under treatment. Many ataxics come to a doctor 
first simply because they cannot easily pass water. When- 
ever that is the case, without local cause for the difficulty, 
always suspect this or a similar condition, and test the 
knee-jerk. In other cases the gastric crises have been 
thought to be due simply to primary gastric disorders. 
These difficulties are chiefly due either to imperfect knowl- 
edge or to incomplete examination. But there are other 
and more excusable diagnostic difficulties which arise from 
the occasional difficulty of distinguishing tabes from allied 
diseases. There are other morbid states which present 
almost the same symptoms. Especially is this true of 
chronic multiple neuritis to which I have already referred. 
When due to alcohol or arsenic it may be manifested by 
pains similar to some of those of tabes, as well as by loss of 
cutaneous sensibility, and also by loss of the knee-jerk, 
and distinct, even conspicuous, inco-ordination. This is 
true, as I have also mentioned, of the ataxic form of dipth- 
theritic palsy, although, in this, pains suggestive of tabes 
are usually absent. But in all these cases the chief indi- 
cation depends upon the detection of the cause, which you 
will seldom have difficulty in discerning, if only your 
scrutiny is properly directed by a knowledge of the possi- 
bility. Often also your opinion will be supported by the 
loss of pupil-action to light, which is so common in tabes, 



154 LOCOMOTOR ATAXY. 

but which is very rare in the maladies that may be mis- 
taken for it. 

Another class of diagnostic difficulties is due to the fact 
that there are cases which present all the symptoms of 
tabes, but others in addition. The most frequent and most 
important of these are cases of general paralysis of the 
insane. As a matter of fact, these patients have tabes ; not 
only are its symptoms present, but its lesion exists ; but 
they have also the cerebral degeneration which causes the 
special symptoms of general paralysis. It is not a question 
of distinction; it is a question of recognising the combina- 
tion. As a rule, also, the common antecedent of pure tabes, 
syphilis, has also preceded the combined malady. 

Thirdly, there are cases which present some symptoms 
of tabes, only others are absent and are replaced by symp- 
toms of a different character. In the malady which we 
term ataxic paraplegia there is conspicuous unsteadiness of 
movement and in standing, but there is weakness as well ; 
the knee-jerk is not lost.; pains are slight; the pupil is not 
affected ; and, as the weakness increases, there is an increas- 
ing tendency to extensor rigidity in the legs; and, with less 
power of movement, its disorder necessarily sinks into the 
background. This malady is due to a combination of scle- 
rosis in the lateral columns of the cord, and in the posterior 
columns in the dorsal region, involving especially the as- 
cending fibres of the posterior median columns, the fibres 
which, as we have seen, probably convey impulses to the 
cerebellum. It does not involve the fibres which convey 
impulses to the grey matter, at the level of origin, which 
subserve the knee jerk. So the knee-jerk is not lost; the 
irritation of the nerves, which causes the pain, and their 
interruption, which causes the anaesthesia and the extreme 
ataxy, are absent. Wanting these features of tabes, the 
cases present the loss of power that is absent in typical and 



UNSATISFACTORY SYMPTOMS. 155 

early tabes, and a sufficient examination, with adequate 
knowledge, renders the nature of the malady clear enough. 

In cerebellar tumour there is unsteadiness which reminds 
us of some cases of ataxy, and of the cases that I have just 
described. But there are not the other leg-symptoms of 
tabes, with one curious, but not frequent exception. Oc- 
casionally, the knee-jerk cannot be obtained in cases of 
cerebellar tumour. It is a curious fact, but we cannot yet 
give a satisfactory explanation of it. It is especially curious 
on account of the association with unsteadiness of move- 
ment in both diseases — an association which is probably 
not accidental, but has a significance at present obscure. 
In cerebellar tumour there is no anaesthesia in the limbs ; 
very often, instead of an absent knee-jerk, this is increased, 
and there is even a foot-clonus from pressure on the pyr- 
amidal tracts ; headache and vomiting are conspicuous 
features, and the latter does not occur in isolated "crises," 
as in tabes. Lastly, optic neuritis is extremely common, 
and atrophy, if found, is distinctly that which succeeds in- 
flammation, and quite different from the atrophy of tabes. 

Lastly, some hysterical girls present some unsteadiness 
in walking, and the question of this disease has arisen. 
But they have no other symptom of tabes. The ataxy 
is trifling and limited to the maintenance of equilibrium. 
It may not be easy for you to conceive that such patients 
should be thought to be suffering from tabes, but this error 
is sometimes rendered more easy by the fact that no knee- 
jerk is obtained. In many cases of hysteria, and, indeed, 
in many perfectly healthy persons, the knee-jerk seems to 
be absent ; sometimes many attempts fail to obtain it. This 
is, however, simply due to the fact that the muscles are not 
relaxed, and a very slight voluntary contraction of the 
flexors prevents the jerk. I believe the knee-jerk is never 
absent unless there is structural disease in muscle, nerve, 
or cord, or (rarely) within the skull. Some fifteen years 



156 LOCOMOTOR ATAXY. 

ago I published a number of cases in which it was absent 
under normal conditions. All I can say now is that I 
should like, very much indeed, to examine these patients 
again, because I have no doubt whatever that I should now 
succeed in eliciting the jerk in every one of them. So, 
when I am told that the phenomenon is absent in a healthy 
person, I venture to doubt the fact, and in doing so I only 
treat the observations of others as I treat my own past 
observations. If the subject shuts the eyes, hooks the 
flexed fingers of the hands together and pulls on them, the 
jerk generally becomes distinct, though before it may have 
seemed absent. In a few, it may be necessary to let the 
legs hang vertically over the edge of a table, and it is 
always well to place your fingers on the hamstring tendons 
to ascertain their degree of relaxation. Yet, with all these 
precautions, I sometimes meet with cases in which I cannot 
obtain it on repeated attempts, and yet, next day, it is pro- 
duced in such typical form as to prove that its absence had 
been apparent only. Regard then with doubt even your 
own observations on cases in which there are no other 
symptoms usually associated with its loss. 

What of the prognosis of this disease ? First, remember 
that the malady involves very little danger to life, however 
extreme it may become, save by exhaustion due to laryngeal 
or gastric crises, or by the insidious development of some 
disease, such as pleurisy, which may not cause the warning 
pain that it produces with normal nerves. But one frequent 
and serious danger to life is directly related to the disease 
— that from the affection of the bladder, and impairment 
of the functions and structure of the kidneys, which I have 
already described. This danger may be prevented. On 
the other hand, unfortunately, actual recovery is even less 
likely than is death. 

The prospect, however, is not so gloomy as this state- 
ment may suggest. I speak of " recovery " in the medical 



PROGNOSES 157 

and accurate sense of the word. Short of the disappear- 
ance of all the symptoms of the disease, they may and 
often do lessen to a degree that is practically unimportant 
to the patient, and they still more often cease to increase, 
and, though continuing, are tolerable. In the majority 
all cases, the disease, carefully treated, is not progres- ive 
This is true at whatever stage it is met with. Only when 
the symptoms are rapidly or steadily increasing (especially 
if this is in spite of treatment) must you be apprehensive 
that the affection will go on to grave disability-. On the 
other hand, in even.- stage you are not justified in holding 
out to the patient the anticipation of more than arrest and 
a slight degree of improvement More may be achieved, 
but you cannot reckon on it In the early stages, arrei: is 
almost tantamount to recover}', so far as the patient's con- 
sciousness is concerned. You cannot say that the patient 
has actually recovered, because if you test the knee-jerk 
even- year for twenty years, you will probably find it still 
absent. But, happily, the loss of the knee-jerk is not a 
symptom which enters into the patient's consciousness un- 
less : 5 assisted there by medical help. The pains, it is 
true, are not likely to leave consciousness untroubled, but 
they often become trifling and can generally be relieved. 

Remember, moreover, in connection with the pains, this 
very important fact, that tabetic pains, however severe, do 
not necessarily mean continued increase of the disorder. 
They seem, once excited, to go on as a neuralgia dees — 
without the morbid process becoming greater. The- are 
merely a persistent effect of the persistent alteration of 
molecular nutrition. 

It is unfortunate that, in considering any disease, we are 
compelled to leave to the last the subject that is first in 
importance — its treatment. I have already told you that, 
in spite of its relation to syphilis, nothing is to be looked 
for from anti-syphilitic treatment. In very rare cases :: 



158 LOCOMOTOR ATAXY. 

early stage and rapid cause, iodide of potassium has 
apparently done some good. In many of these its influ- 
ence has been combined with that of other agents, and it 
sometimes does good in diseases that are not related to 
syphilis. Certainly your experience will soon demonstrate 
to you the accuracy of the general statement I have made. 
But if nothing is practically to be looked for from anti- 
syphilitic treatment, much is to be dreaded from its ener- 
getic use. When a patient has passed the stage of active 
syphilis, and is suffering from the sequelae due to its re- 
sidual influence, such treatment, and especially mercurial 
treatment, seems to intensify the tendency of the nerve 
elements to degenerate. I have seen some disastrous cases, 
in which a grave affection of this character has immedi- 
ately followed a thorough course of mercurial treatment, 
what they call abroad a " cure " — a term which bears to 
us more unconscious irony than it does to those who 
employ it. True, in many cases it may be wise to give the 
patient, for a few weeks, some iodide of potassium, because 
he is sure to be told that he ought to have had it, and it does 
not produce the harm of thorough mercurial treatment. 
It is often well to clear the therapeutic ground of any pos- 
sible source of future, though baseless, feeling that any- 
thing has been neglected, provided the measure involves no 
harm to the patient. Moreover, that which is true of full 
doses of mercury is not true of small doses. There seems 
to be some truth in the assertion that very small doses of 
mercury have a tonic influence on patients who have had 
syphilis, but who have ceased to be actively syphilitic. 
Such doses may, therefore, often be wisely given in com- 
bination with other agents. But, in treatment by drugs, it 
is essential to realize the fact that the state and process you 
are striving to modify and arrest is essentially a degenera- 
tive process, a process of defective nutrition, tending to 
structural decay. As far as we can discern, it presents no 



TREATMENT. 159 

difference from the similar condition that is due to other 
causes. Further, the medicinal agents that sometimes 
exert a distinct influence on the process, seem to do so 
irrespective of its causation. Among these agents the 
first place must be given to arsenic. Its influence is, in 
many cases, conspicuous to no one more than to the suf- 
ferer. It is very interesting to note that we may trace a 
reason for the effect in the fact that arsenic has been 
proved to influence the nutrition of the peripheral nerves, 
especially the afferent nerves of the skin, which conduct 
sensation, and which also, as we have seen, determine 
nutrition ; probably it has a similar influence upon the 
deeper afferent nerves. It has to be continued, however, 
for two or three months, and then, after one or two months 
omission, it may, with advantage, be resumed. The form 
may be either the liq. arsenicalis, or liq. arsenici 
hydrochlorici, in a neutral or acid mixture, respectively, or 
the arseniate of soda in a pill. Phosphorus, which has so 
many points of similarity to arsenic, may be given alter- 
nately, and strychnia or nux vomica may be combined 
with either. 

Next in value to arsenic I am inclined to place a drug 
which I have used in many cases — seldom without benefit 
— chloride of aluminium. I do not know whether it has 
been used by others in such cases. It seems to have a 
combined tonic and sedative influence on the structures 
affected. Only yesterday I had a letter from a doctor 
about a patient who said he had been taking chloride of 
aluminium some time ago with great benefit, but had 
lately been trying a number of things. The doctor in- 
formed me that with none of these did he get any improv- 
ment, rather, his walking and his pains became worse, but 
as soon as he resumed the chloride of aluminium he 
again began to improve. It seems to have an especial 
effect in lessening the tendency to the pains. The dose is 



160 LOCOMOTOR ATAXY. 

two, three, or four grains twice or three times a day after 
meals. It is fairly soluble, and you may give it in combi- 
nation with belladonna, Indian hemp, or nux vomica. 
Other tonics, as quinine, and sometimes iron, may be 
given with advantage in combination with arsenic or 
aluminium. Paroxysms of pain are most effectually 
relieved by antipyrin or acetanilide (once called anti- 
febrin). When superficial they are usually lessened by the 
application of chloroform to the skin, and very certainly, 
for several hours, by the hypodermic injection of cocaine 
at the upper part of the area of the skin to which they are 
referred. It does not influence the deep pains. 

No other local measures are of distinct use. Elec- 
tricity is not generally of service. If, indeed, the muscles 
are energetically faradised, so as to stimulate and wake up, 
as it were, the afferent nerves, the patients seem afterward 
to walk a little steadier ; but I have not been able to feel 
sure that permanent good has resulted from a course of 
this treatment. 

These, then, gentlemen, are the chief points with regard 
to the disease, to which I desired to direct your attention. 
I must hope that the facts I have mentioned, whether any 
of them are new to you or not, may be, at any rate, fixed 
in your minds by the relations I have pointed out, and 
those which have a direct relation to practical medicine 
may prove of service. 

We will now look again at the two patients whom we 
saw last week, and examine them in the light of what I 
have been saying to-day. 

I here show you the patient with the remarkable affec- 
tion of the cranial nerves — to an extent, indeed, that we 
very seldom see. He has, as you observed last week, 
considerable ataxy, loss of knee-jerk, loss of sensation ; 
he has even some loss of sensation in the region of the 
fifth nerve. His pupils are large, and do not act to light 



CLINICAL CASES. 161 

or to accommodation. Accommodation is probably para- 
lysed. There is weakness of the right and left external 
recti muscles. The eyes are raised fairly well. The left 
converges much better than the right, although the right 
moves well in the lateral movements, — an illustration of 
the distinctness of the centres for the movement of the in- 
ternal rectus, with its fellow, in convergence, and that with 
the external rectus, in the lateral direction. There are 
conspicuous hollows in the position of the muscles of 
mastication, the temporals and masseters, and you can 
hardly feel any muscular contraction there. The motor 
branch of the fifth nerve on each side has evidently de- 
generated in extreme degree. The tongue is protruded 
well. He cannot bring his lips perfectly together, in con- 
sequence of weakness of the lower part of his face. He 
closes his eyes fairly well. He seems to close his glottis 
(as you observe by the explosive cough), although one 
of the vocal cords was found not long since to be 
paralysed. 

In the second patient there is a remarkable defect of 
sensibility upon the chest. He is suffering from the form 
of tabes to which I have already referred, in which there 
is greater damage to the nerve roots in the dorsal than in 
the lumbar region, so that there is a wide band of anaes- 
thesia around the thorax. He has no pain, only tightness 
round the chest. The irritation in the nerve roots has 
only caused this sensation of constriction. This sensation 
occurs very frequently when the root fibres are damaged 
and irritated by other processes. It is not a rare symptom, 
however, in locomotor ataxy, so that you must not im- 
agine, because you meet with it, that there is necessarily 
any focal lesion of the cord. 

Just below the nipple he ceases to feel a touch. 
Between the nipple and the umbilicus there is anaesthesia 
on the right side, but only in a much narrower band on 



1 62 LOCOMOTOR ATAXY. 

the left. There is also a more extensive, wider affection 
of the nerves of touch than of the nerves of pain. In the 
first patient there was a loss of the plantar and cremas- 
teric reflexes, in the second the abdominal reflex should 
be lost in a greater degree on the right side than on the 
left. (On examination this was found to be the case.) It 
is distinctly greater on the left side, on which the sensation 
of touch has suffered most impairment. The loss of 
reflex action from the skin is related in greater degree to 
the loss of tactile than to that of painful sensibility. 

Here I must stop. Let me beg you, however, to go on. 
Supplement any new knowledge you may have gained to- 
day by reading a systematic account of the disease ; strive 
to connect the facts you thus learn with those you have 
just observed; and, above all, let the knowledge give 
point and effective power to the observation of the cases 
that are sure, sooner or later, here or elsewhere, to come 
under your notice. 



LECTURE XI. 
THE FOOT CLONUS AND ITS MEANING. 

Gentlemen : — The patient before you presents an unusual 
degree of increase in the symptoms associated with the 
name " tendon reflex," of which the knee-jerk and foot 
clonus are our special types. I have lately had occasion 
to draw your attention to the loss of these processes, and 
to the relation of the loss to the inco-ordination with 
which it is so often associated. The features of the excess 
of these phenomena, which I am going to show you, sug- 
gest that we may wisely consider their excess in relation 
to their nature. The process on which they depend has 
been, in my opinion, widely misunderstood, and a correct 
conception of its nature makes clear to us much that 
would otherwise be obscure. It is worth while, therefore, 
to consider its character, although in doing so we shall 
have to traverse ground familiar to many of you. I find, 
however, by experience, that the knowledge supposed to 
be familiar is often in a confused and shapeless state, and 
it is as useful to reconsider such a subject as it is to pre- 
sent the actual novelties that are welcomed with much 
more eagerness. 

What is the knee-jerk ? When the leg is in a certain 
posture, a tap upon the patellar tendon makes the muscles 
contract that end in it ; and, when the foot is in a certain 
posture, a tap on the Achilles tendon makes its muscles 
contract. It was at once assumed, not unnaturally, that 
the tap stimulated the nerves of the tendon, and that the 

Medical Magazine, Vol. IV., May, 1 895. 
163 



1 64 THE FOOT CLONUS AXD ITS MEANING. 

contraction of the muscles was a reflex action. At that 
time, however, the presence of nerves in the tendon had 
not been ascertained by the microscope ; the name em- 
ployed, however, involved their existence. A " tendon- 
reflex" action could not occur unless the tendons contain 
nerves. Hence, the point was at once investigated and 
the result was to prove that there are nerves in the tendon. 
Bat their investigations were wholly unnecessary to estab- 
lish the fact. May I ask each one of you now present to 
compress suddenly your Achilles tendon between the 
thumb and finger? If the squeeze is energetic you cannot 
possibly need the microscope to prove the presence of 
sensory nerves in the structure. The discovery, there- 
fore, that nerves could be seen in tendon was super- 
fluous, but it supplied the needful evidence that there was 
a mechanism for a "tendon reflex," and so it seemed to 
confirm the view that the contraction referred to is a reflex 
action. That opinion was embedded in the term "tendon 
reflex," and it has persisted to this day — a curious in- 
stance of the manner in which a name founded upon a 
theory may perpetuate the theory although it has been 
proved to be untenable. Within a year of these observa- 
tions, it was shown to be impossible that the contraction 
could be a true "tendon reflex." As you know, it is to 
be obtained in animals as well as in man. Tchirjew com- 
pletely isolated the patellar tendon ; he divided all its con- 
nections except those with the bone. He divided every 
nerve, and he found that this made no difference whatever 
to the effect of a tap on the tendon. That is an instance 
of the absolute facts of science, of the facts that cannot be 
got over. It alone shows that to whatever the phenomena 
are due they are not contractions due to the stimulation of 
the nerves of the tendon. 

There is another interesting observation that bears on 
this point and can be easily demonstrated. When there is 



WHAT IS THE KNEE-JERK? 165 

moderate increase of these contractions, if the foot is 
gently pressed up so as to make the Achilles tendon a 
little tense, the muscular contraction can be obtained as 
well by a tap on the edge of the tendon as on the posterior 
surface. If the tendon, when tapped on the side, is sup- 
ported on the opposite side (by fingers against it), so that 
the tendon cannot move when tapped, no contraction occurs. 
Tap gently the tendon so supported, and then remove the 
support and tap again with the same force : the first tap 
has no effect, the second tap causes a contraction. The 
difference is that in the one case the tendon moves before 
the blow, in the other it does not. That is, unless the tap 
increases the tension on the muscle, it has no effect. 

This fact proves that the effect must be due to the in- 
creased tension, acting either on the muscle or on the 
tendon itself by its nerves. But the experiment I referred 
to, in which all connections of the tendon were divided, 
shows that it cannot be due to any effect on the nerves of 
the tendon, therefore the contraction must be due to the 
increase of the tension of the muscle. The result has 
never been disputed, it proves that the tap on the tendon 
acts through the muscle and not through the tendon nerves. 
With this fact we are able better to perceive the significance 
of another. We can only obtain these contractions when the 
limb is in such a position that the tap on the tendon in- 
creases the tension of the muscle. If the muscle and ten- 
don are relaxed the tap has no effect. There must be such 
a degree of tension as to enable the tap on the tendon to 
increase the tension of the muscle, or no contraction 
occurs. 

Let me here divert your thoughts to the fact I have 
recently pointed out to you in connection with locomotor 
ataxy, the fact that the muscle nerves are stimulated by 
two mechanical processes — by compression and by ex- 
tension. 



166 THE FOOT CLONUS AND ITS MEANING. 

You may remember that I mentioned to you that it is the 
extreme compression of the over-contracting fibres that 
gives rise to the pain of cramp, and that when the muscle 
nerves are rendered hyperaesthetic by the effect of the 
cramp it is by tension that the pain is produced. The pain 
by compression during cramp, and the pain by tension in 
the after-state, afford us a most instructive illustration of 
the two modes in which these different muscle nerves are 
stimulated. We are, in general, unconscious of their exist- 
ence, their stimulation gives rise to no sensation. I use 
the term " afferent " because they do not normally influence 
consciousness. They are not " sensory." Nevertheless, 
the impulses act upon the motor centres in the cord, and, 
probably, also on the centre in the cerebellum influence 
their action by the state of tension or contraction of the 
muscle. 

To revert to our local "phenomena; " it is thus in har- 
mony with what we have learned in other ways that this 
sudden increase of tension should act upon the muscle and 
muscle nerves. The effect of a blow on the tendon is pro- 
duced through the muscle. So far as it is reflex, it is a 
muscle-reflex action, and not a tendon-reflex action. There 
may be error of name; that is, alone, of little consequence. 
You may call a pen by some other name without interfer- 
ing with its use, but it is different if the name involves a 
theory. You cannot use these phenomena, as an aid to 
understanding disease, if you call them " tendon reflex." 
At least it is necessary for every one first to unlearn the 
erroneous idea contained in the name, and, as a fact, a large 
number of persons never unlearn it and never gain the clear 
perception they might acquire of other phenomena of dis- 
ease. 

Let me now try to show you that a certain tap on the 
tendon is effective only when it can increase the tension 
of the muscle. In this patient, suffering from hemiplegia, 



MYOTATIC CONTRACTIONS. 167 

I press up the foot. Unless the foot is pressed up so 
as to make the muscles tense a contraction cannot be 
obtained. For it, there must be gentle tension. Hence I 
have called the phenomena " myotatic " or " tense-muscle " 
contractions. When in excess, and the muscles are made 
tense, the very slightest sudden mechanical influence pro- 
duces the needful stimulation. I very gently tap the 
tendon from the side, first without support on the other 
side, and then supported by the finger tips so that the tap 
does not displace the tendon. You note that the tap, 
which in the first instance caused contraction, has no effect 
when the tendon cannot move — that is, when the tap cannot 
suddenly increase the tension on the muscle. You see the 
difference is clear. This fact, taken in conjunction with 
the other fact I mentioned, though the division of the 
nerves of the tendon prevents it, makes certain the fact 
that the increased tension does act upon the nerves of the 
muscle. 

Then comes another question which is, however, com- 
paratively unimportant. Is that contraction an immediate 
reflex effect of the stimulation of the afferent nerves of the 
muscle ? It is a difficult question, and the answer depends 
on difficult time measurements. When the interval be- 
tween the tap and the contraction is carefully measured it 
is found to be shorter than that which we can well con- 
ceive can be that of a reflex action. But I must ask you 
to allow me to pass this by. It seems to me probable that 
each contraction is not reflex. But this has nothing to do 
with the exclusion of the tendon nerves as the source of 
the afferent impulses. Yet I shall ask you to let me assume 
the theory that each contraction is not reflex, because I can 
better thus put before you the general principles on which 
I desire to insist, which help us most to understand the 
phenomena of disease and of health, and of which this 
special point is only one unessential element. 



168 THE FOOT CLONUS AND ITS MEANING. 

Far more important than that is the way in which the 
theory I am about to mention harmonises with other facts 
and illustrates many phenomena of disease. We only get 
these contractions when the muscle is in a certain state of 
tension, and the theory I refer to is that that tension, by 
gently stimulating the afferent nerves of the muscles, in- 
duces a state of the muscular fibres in which they are 
excessively sensitive to the mechanical influence of the 
suddenly increased tension of the tap. The gentle tension 
causes the irritability. The irritability is reflex ; the con- 
tractions are local, and would not occur were it not for the 
irritability which is reflex. 

In connection with this, two other facts are of impor- 
tance. First, there is the condition called muscular " tone " 
or " physiological tonus," the curious state of slight con- 
traction of the muscle by which the muscle is always 
adapted to its posture, and always maintains a certain 
amount of contraction whatever the proximity or distance 
of its attachments. This depends upon the spinal cord. 
If the motor nerves are divided it ceases instantly ; it 
ceases instantly also if the sensory nerves are divided, and, 
therefore, it must be a reflex process. It is probable that 
this muscular tone, when a little augmented by an increased 
afferent impulse from tension, is the irritability which 
makes the muscle contract in response to the local stimula- 
tion. In most instructive harmony with this we find that 
whenever these phenomena become excessive, there is a 
tendency to tonic spasm, which is seen in such striking 
degree in spastic paraplegia, and, as you know, is always 
accompanied by such conspicuous excess of these contrac- 
tions. Compare the light which that throws on the symp- 
tomatic pathology of spastic paraplegia with the absolute 
darkness in which the " tendon-reflex " theory would leave 
it ; if, indeed, it were conceivable that the tendon-reflex 
theory could be held by any one who knows the facts. 



HOW PRODUCED. 169 

But the name " tendon-reflex " goes on and conveys its 
theory to those who know nothing of the subject except 
the name, and thereby hinders them from all perception of 
the really instructive elucidation conveyed by the alterna- 
tive term the "muscle-reflex action." Therefore I never 
use the term " tendon reflex," nor have I done so for many 
years. I use the term " muscle reflex," or the general 
term which I have mentioned, " myotatic." That word, 
however, has not become much used. I am, however, 
consoled by the different fate of another term I suggested 
at the same time. At the meeting of the British Associa- 
tion at Cambridge I was talking with Professors Clifford 
Albutt and Westphal about the error of the term " tendon 
reflex " — which Westphal (who first pointed out the im- 
portance of the symptom) had always avoided. He pre- 
ferred the name " knee-phenomenon." I asked, "Why 
not call it the ' knee-jerk ' ? " Clifford Albutt so emphati- 
cally approved the term that I took the first opportunity of 
setting it going, and its use immediately became universal. 

The contraction which follows the tap is an instanta- 
neous one. The increased tension acts on all the fibres of 
the muscle; all contract. It is an instance of a simul- 
taneous single contraction of muscular fibres. When 
there is maintained contraction of a muscle, it depends 
upon the fact that a similar contraction occurs in different 
fibres not simultaneously, and the contraction is main- 
tained because there is never a moment in which a large 
number of fibres are not contracted. Clonic contractions 
are simultaneous ; tonic are not. 

If the muscular irritability excited by tension is con- 
siderably increased, and the tension is suddenly applied, it 
causes a single contraction ; as this ceases, the excitability 
of the muscle is renewed, and, if the tension is maintained, 
contraction occurs. That is the reason why, by main- 
taining the tension upon the muscle, a clonus is produced 
'5 



170 THE FOOT CLONUS AND ITS MEANING. 

— a foot clonus or a rectus clonus. There is no essential 
difference between clonus and the knee-jerk, except that 
the irritability must be excessive to permit a clonus to be 
obtained. 

The patient whom I now show you, has an extreme 
excess of this irritability. Before pointing out its features, 
I may mention the conditions under which it becomes 
excessive. You remember what I said recently regard- 
ing the impulses from the muscles in locomotor ataxy, 
and the way in which their loss deprives the spinal 
centres and the brain of the guiding impulses which 
depend upon the state of the muscles, and so disturbs 
co-ordination. I indicate on the black-board, in the 
diagram before you, a couple of muscular fibres, and the 
connective tissue between them, and from between them a 
couple of afferent nerves fibres going up, through the 
ganglia on the posterior root, to the spinal cord. These 
fibres have different destinations. One passes through the 
postero-external column, ascending in it to the medulla, 
where it en'ds in grey matter, whence a path continues it 
to the middle lobe of the cerebellum; there its impulses 
are combined with others to guide the motor cortex of 
the brain. If the nerves are degenerated, the postero- 
median column degenerates up to the medulla. The other 
fibre seems to pass into the posterior cornu, and there, 
probably dividing, comes into relation with the processes 
of the motor cells, from which a motor fibre passes down 
to the muscle. This afferent fibre, acting on the motor 
cell, is a type of the fibres which determine what I call 
the muscle-reflex action, that is, from the muscle to the 
muscle. These determine the physiological tone and 
determine also the excitability manifested in the knee-jerk 
and, when excessive, in the clonus. But the motor cells 
form part of the voluntary path from the brain. This 
descends in the lateral column, in the " pyramidal tract," 



FUNCTION OF AFFERENT FIBRES. 171 

the fibres of which seem to end by branches that are 
related to those of the motor cells ; thus the pyramidal 
fibres act through the motor centres of the cord, which 
are also influenced by the impulses from the muscles. 
We cannot say how much these afferent muscular im- 
pulses do in determining the form and degree of the 
action excited from the brain. They probably have a very 
great influence in facilitating the arrangement of muscular 
contractions, especially in standing and walking. Yet 
these pyramidal fibres acting on the motor centre seem 
also to restrain its reflex activity. We should not know 
this if it were not for the effect of the loss of those fibres 
when the pyramidal tracts are destroyed. There is an in- 
crease of the muscle-reflex action and of all the pheno- 
mena by which it is manifested. As you know, in such a 
case we have an excessive knee-jerk, but that excessive 
knee-jerk does not develop at once. If the cord is 
divided, there is instant excess of the superficial reflex 
action of that from the skin, but it is some time before 
there is excess of the muscle-reflex action, and it after- 
wards gradually increases. It seems as if the function of 
the pyramidal fibres was to exert a continuous gentle 
restraint on the muscle-reflex centre. When that influ- 
ence is withdrawn, there is a gradually progressive 
augmentation, a sort of functional hypertrophy, of the 
muscle-reflex action, which leads first to excessive knee- 
jerk, then clonus, then gradually increasing spasm, and 
then to the full condition of spastic paraplegia. At last 
there is a condition of spasm so intense as to prevent the 
contractions being obtained. 

I shall take some other opportunity of speaking of the 
fallacies there are in obtaining evidence of the presence of 
the knee-jerk when it is normal. I wish now to show you 
this remarkable feature of the excess of this muscle-reflex 
irritability. The patient before you is a man who has had 



172 THE FOOT CLONUS AND ITS MEANING. 

myelitis in the dorsal region of the cord. I need not trou- 
ble you with his history. His symptoms afford evidence 
of perfect integrity of the lumbar enlargement, except for 
the secondary degeneration of the pyramidal fibres, due to 
the effects of the inflammation higher up. They have to 
some extent recovered, and can perform their function of 
conveying the voluntary impulse, so that he is able to 
move his legs, but so imperfectly that he is still unable to 
stand without support. He has much extensor spasm in 
his legs, the result of the excess of this muscle-reflex action, 
and the degree of this excess is manifested in a feature that 
is not often to be observed. Xot only is a clonus in the 
extensors of the ankle, the calf muscles, produced instantly 
by the gentlest passive flexion, but when he flexes the 
ankle himself, by voluntary contraction of the flexor mus- 
cles, the tension of their opponents sets up clonus in them. 
The ordinary way of obtaining clonus is suddenly to make 
the muscles tense, and the tension develops irritability and 
produces contraction without there being any interval which 
you can appreciate. But, as I have explained, when the 
first contraction is passing off, the maintained tension acts 
as a stimulus to another, and the time of each contraction 
is such that their frequency is about 6, 8 or 9 per second. 
When the patient flexes the joint you see there is developed 
a characteristic clonus, quite like that produced by passive 
tension. It is a feature you will seldom see, although I 
confess I cannot tell you why it is so rare for voluntary 
movement to do that which passive movement does so 
readily. 

It is, as a rule, only in the muscles of the calf that a 
clonus is obtained, not only because they are conveniently 
made tense in this way, but also because in them this re- 
flex action is normally very active and important. You 
may often get a clonus in the muscles which move the foot 
laterally, and also in the rectus femoris when the patella is 



ITS DIAGNOSTIC SIGNIFICANCE. 173 

pressed towards the foot. I now press the patella straight 
down towards the foot and then tap it in the same direc- 
tion. You see that then a well-marked clonus is developed. 
When the patient is horizontal you can obtain the knee-jerk 
quite readily by depressing the patella and then giving a 
tap on the depressing finger in the direction of the patella, 
but not unless it is in slight excess. 

Not only can a clonus be obtained in the peronei ; I 
have even got it in the muscles of the great toe. It is often 
to be obtained in the flexors of the fingers in cases of hemi- 
plegia. I have even found it in the trapezius. 

With two other practical remarks I will conclude. 
First, remember that when a patient is in bed the best way 
of testing the knee-jerk, provided that you are unable to 
get it by pressing the tendon in the way described, is to 
let the hip and knee be flexed, and to let the foot rest upon 
your hand quite passively, and then the leg is in the most 
convenient position, with just the right amount of tension 
for the production of the contraction. This method is of 
extreme value in testing the knee-jerk. 

The other fact is that whenever the excess is in such 
degree as to enable the clonus always to be obtained, that 
is, when the irritability is so great that the continued ten- 
sion acts as a stimulus after each contraction, there is cer- 
tainly nutritional change in the muscle-reflex centre — there 
is persistent functional excess such as implies a nutritional 
change. This nutritional change is important. There has 
been much discussion as to the significance of a definite, 
distinct clonus, independent of any voluntary contraction of 
the calf muscles, such as you can readily perceive. I am 
certain of this, that for one case of error due to clonus being 
thought to be due to organic disease, when it was really 
due to a so-called functional state, twenty cases of error 
have arisen in consequence of the clonus of organic disease 
being disregarded, its significance being underrated. I 



174 THE FOOT CLONUS AND ITS MEANING. 

could give you a long list of very instructive illustrations 
of the errors into which disregard of the foot clonus has 
led distinguished physicians. 

Yet one other point. In spite of the significance of such 
extreme increase as you observe in this patient, as proof of 
structural disease, it is no proof of irrecoverable disease. 
Never have I seen such intense excess, with such intense 
spasm, as was presented by a patient of whose case proba- 
bly most of you have heard, and in whom there was abso- 
lute motor and sensory paraplegia up to the level of the 
ensiform cartilage. In spite of the absence of cutaneous 
sensibility there was that terrible excess of the sensibility 
to the deep-seated pain of muscular spasm, so that the con- 
tractions caused an agony of such intensity that the man 
must have died of sheer pain in three months' time. The 
symptoms were due to a tumour pressing on the spinal 
cord ; the tumour was removed, and that patient has been, 
for years, free from the slighest trace of increase of knee 
jerk, or spinal symptoms of any kind. He daily walks 
miles, pursues an active life, and is the head of a big manu- 
facturing firm. Ten years have now elapsed since he was 
in the condition I have described, and his case should im- 
press on you the fact that no excess of myotatic irritability, 
and no degree of clonus or of spasm, preclude the possibil- 
ity of recovery. 



LECTURE XII. 

A CASE OF SYRINGOMYELIA. 

Gentlemen: — As the changed conditions of my work 
here prevent me from continuing the out-patient clinics 
which I have carried on for many years, I propose to try to 
find some substitute for them in showing you a case each 
Wednesday afternoon, and endeavouring to extract from 
its facts such information and instruction as it will yield 
us. 

I begin to-day with an example of an uncommon disease. 
Let me, at the outset, warn you against the frequent error 
of thinking that a rare disease can only yield you know- 
ledge which will be rarely needed. It is not so. Diseases 
which are uncommon cannot be studied without consider- 
ing common facts and without giving increased ability to 
recognise diseases which are often met with. 

The patient before you came into the Hospital a few 
weeks ago, presenting, as he presents now, two chief sets 
of symptoms : he has extensive loss of sensation over the 
hands, arms, and parts of the trunk and legs ; he has also 
muscular weakness, and muscular wasting in the right 
hand and forearm, and a little weakness in the left. 

The diseases in which loss of sensation is the chief 
symptom are not numerous. You meet with it as an iso- 
lated symptom in functional anaesthesia, in hysterical 
hemianesthesia, for instance ; you find it also in some 
cases of organic diseases of the brain which cause hemi- 
anaesthesia, and you meet with it in organic disease of the 

Delivered May io, 1893. Clinical Journal, May 31, 1893. 
175 



176 A CASE OF SYRINGOMYELIA. 

nerve trunks. But in all these forms, each kind of sensa- 
tion is involved ; the tactile sensibility is usually impli- 
cated even in greater degree than sensibility to pain. But in 
this patient — as in most other cases of the kind — the loss of 
sensation presents the remarkable feature that it involves 
sensibility to pain, and involves sensibility to temperature 
— to heat and to cold — but does not involve sensibility to 
touch. Such a combination, with the exclusion of tactile 
sensibility from impairment, is met with only in one other 
morbid process — degenerative changes in the peripheral 
nerves ; such, for instance, as are met with in many cases 
of tabes, and in a few cases of alcoholic and other forms of 
neuritis. In these, also, you may have sensibility to pain 
lost, sensibility to touch persisting, but their characteristic 
is that they involve the extremities of the limbs, either 
alone or in preponderant degree, and do not extend far up 
the limbs toward the trunk. But, in this case, and in 
other cases of the kind, the loss of sensation extends over 
the whole upper limbs, and involves a considerable portion 
of the trunk. Not only does it exist on the hands and 
fingers, but upon the chest as far as the fourth cartilage ; 
it involves the neck and even the back of the head as far 
as the cervical nerves are distributed ; it involves, in front, 
the lowest part of the abdomen on the right side. It also 
extends (an unusual feature) over the front of the thigh as 
far as the knee ; and behind — a point to which I ask your 
special attention — it is found over the whole sciatic area. 
Thus you see, by its distribution, it is entirely distinct from 
the only other morbid state in which this special loss is 
met with. 

Let me show the facts I have described. I prick the 
patient on the palms and fingers and arms with a point, and 
you hear that he feels it only as a touch. So also on the 
chest, but you perceive that on the left side this condition 
does not extend quite so far down as on the right side. We 



LOSS OF SENSATION AND MUSCLE-POWER. 177 

examine the thermic sensibility by test-tubes containing 
hot and cold water. On the arms we find that he is unable 
to recognise either heat or cold, merely feeling the contact 
of the tube ; he has some recognition of heat on the upper 
part of the chest and the back, but not of cold. If we 
were to examine the leg we should find that the condition 
is essentially the same. Note the instructive fact that the 
sensitiveness to cold may be lost when that to heat is not ; 
it confirms the opinion that these two forms of thermic sen- 
sibility are subserved by different nerves. 

The second symptom which he presents is the muscular 
atrophy in the right hand. Observe the peculiar posture 
of that hand ; those of you who are familiar with the effects 
of muscular paralysis will recognise the position as that 
characteristic of paralysis of the interossei. The last two 
joints of the fingers are considerably flexed by the unop- 
posed action of the muscles which bend those joints, the 
long flexors; when he attempts to straighten the hand — to 
extend it — you see the effect in still more marked degree ; 
he cannot extend the middle or last joints of the fingers; 
he is able to extend the metacarpo-phalangeal joints by 
means of the long extensor, but the power of flexing these 
joints, and of extending the others, due to the interossei 
and lumbricales, is lost. This shows some weakness also 
in the long extensor. He is not able to extend the wrist 
together with the fingers. When he closes his fist, how- 
ever, the wrist can be well extended, because then the 
special wrist extensors are active, while they are inactive in 
extension of the wrist and fingers together. You see, more- 
over, the distinct wasting of the thenar and hypothenar 
muscles, and the hollow interosseal spaces, in striking con- 
trast with those of the other hand. 

We will now see what the electrical irritability of the 

muscles is ; this will tell us the state of nutrition of their 

nerves as well as that of the muscular tissue. You see 
16 



178 A CASE OF SYRINGOMYELIA. 

that a moderate faradic current causes contraction in all the 
muscles of the left hand and forearm, but in those of the 
right hand no contraction can be obtained with even a 
strong current. There is loss of the excitability that de- 
pends on the nerves within the muscles ; their state cor- 
responds with that which exists higher up their course, and 
if we test the nerve-trunks that supply these muscles we 
find their fibres equally insensitive. They have undergone 
degeneration. If we apply voltaism to them they are 
equally irresponsive. If we apply it, however, to the 
muscles themselves, we obtain a contraction, because to it 
the muscular fibres can react ; they do so, for instance, in 
the interossei, but only to a very strong current, and in the 
thenar and hypothenar muscles we get no response. There 
is thus a diminution of nerve and muscle irritability cor- 
responding to the wasting, with persistence of a very slight 
excitability in some of the muscular tissue. It is a condi- 
tion that results from, and is evidence of, a slow degener- 
ation of the motor nerves, such as results from slow gradual 
damage to their nerve cells in the spinal cord. 

This disease affords us a striking illustration of the 
great increase of diagnostic power that has come from the 
union of pathological and clinical observation. From its 
clinical characters it would not be possible to infer the 
exact nature of the lesion ; and what may seem more 
strange, however familiar we might be with the pathological 
change, if we knew it alone, we should be unable to infer 
from it that such symptoms would be produced as are 
present in this patient, and which attend the morbid pro- 
cess in the majority of cases. But let us see how far a 
study of the symptoms can lead us. Such an extensive 
differentiation in the loss of the different forms of sensibil- 
ity can have only one meaning. We have seen that it 
does not occur in degeneration of the terminations of the 
nerves in that distribution which we perceive in the case 



COMBINED STUDY OF SYMPTOMS. 179 

before us. It does not occur in disease of the nerve trunks, 
which causes a general loss, corresponding to their distri- 
bution. But in the spinal cord we know that the paths for 
pain and touch are separate, because we know that various 
lesions of the cord — traumatic lesions, for instance — not 
uncommonly involve sensibility to pain, and leave sensi- 
bility to touch unaffected ; and we know also that the path 
of temperature must be near that of pain, because the two 
forms of sensibility are so frequently involved together. 
Therefore we can infer that there is probably a lesion of 
the spinal cord so situated as to implicate the paths of 
pain and of the thermic sense, and not that of touch. 
Beyond this we could not go except to infer, from the 
gradual progress of the symptoms — to which I shall refer 
later on — that it must be a lesion of chronic course. But 
the combination of clinical and pathological observations I 
have mentioned, has shown the remarkable fact that in 
most cases in which this combination of symptoms is met 
with, in any distinct and characteristic degree, the obtru- 
sive pathological feature of the morbid state of the spinal 
cord is the presence of a cavity or cavities within it. The 
disease is that which is currently known as " syringomye- 
it is sometimes called hydromyelia, but there seems 
a tendency to use the term syringomyelia to the exclusion 
of the other. These tendencies of nomenclature, I may 
remark in passing, are so strong that it is generally useless 
to attempt to oppose them ; we have to accept that name 
which is generally adopted, although the term " syringo- 
myelia," since it comes from a word meaning " trumpet," 
is not a very apt one. 

Cavities in the cord, most of which give rise to symp- 
toms more or less similar to those before you, are very 
various. The most common and the most typical is the 
dilatation of the central canal. It may be slight, and then 
may cause no symptoms ; it may be great, so great as to be 



180 A CASE OF SYRINGOMYELIA. 

equal to the normal area of the cord, and by the pressure 
it exerts it may reduce the tissue of the cord to a narrow 
layer surrounding it. Lower down, there may be a normal 
central canal, or a central canal which is closed by a mass 
of nuclei, a condition which is often met apart from any 
disease. In other cases, with a normal or a closed canal, 
behind the posterior commissure there is a cavity — a slit- 
like cavity — between the two posterior columns, extending 
almost to the posterior surface of the cord. You will see 
examples of both forms under the microscopes. Further, 
we may have slit-like cavities, more or less distended and 
widened, in each postero-lateral column, or sometimes in 
one only. Similar cavities may be found within the sub- 
stance of the posterior horn, extending from the front to 
the back of the horn. Among the sections for your ex- 
amination are examples of both these changes, fissures in 
the posterior columns, in both posterior cornua, and in one 
only. Sometimes we find small slit-like cavities in the 
posterior part of the lateral columns, and of these also 
you will find an instance. We may even have a cavity, on 
one or both sides, at the inner part of the middle portion 
of the grey matter, near the base of the anterior cornu ; 
and by its enlargement, such a cavity may come to occupy 
a large part of the place which should be occupied by the 
anterior horn and its nerve cells. 

But another most important fact is illustrated by these 
sections and is generally to be observed. The cavities are 
not the only pathological feature. If you examine them 
closely, you will see that they are bounded by a layer of 
tissue different from that of the rest of the cord, a tissue 
resembling that which lies on each side of the central 
canal, and which occupies the furrow at the side of the 
posterior nerve roots, and which lies also in a thin layer 
between the pia mater and the cord, and is continuous with 
the neuroglia which penetrates and ramifies among the 



ORIGIN OF THE CAVITIES. 181 

nerve fibres of the white columns. It is a relic of the 
embryonal tissue of the cord. It is similar to that of which 
the embryonic cord is composed, and which, in the process 
of development, slowly changes to nerve elements — nerve 
cells and nerve fibres. The presence of this embryonic 
tissue is evidence of the important fact that most of the 
cavities, certainly all those around which it can be recog- 
nised, and probably some others, are due to an arrest of 
development. They are due to the persistence of the early 
cavities, or to the breaking down of persistent embryonal 
tissue, or to both processes. This conclusion is confirmed 
by some other histological features which are found in the 
cases in which there is a distinct layer of this neuroglial 
tissue, and which may be sometimes found when this layer 
cannot be clearly seen, especially a peculiar sinuous mem- 
brane lining the cavity, or peculiar fringe-like processes 
extending outward from such a membrane. 

The origin of most cavities in arrested development is 
thus evident from their features. In the posterior commis- 
sure the epithelial lining may show that a cavity is the 
dilated canal. The embryonal groove is, you will remem- 
ber, at first closed at the posterior surface only; some cavi- 
ties seem to represent an arrest of development at that 
stage, because the cavity due to the enlarged central canal 
extends backwards up to the surface of the cord. In other 
cases, as in one under the microscope that I have already 
mentioned, the closure of the original cavity behind the 
central canal, to form the posterior commissure, has taken 
place, and then an arrest has occurred, so that the cavity 
is between the two posterior median columns. When a 
slit-like cavity is in the posterior part of the lateral columns, 
and sometimes in the posterior horns, or in the lateral 
columns, the adjacent neuroglial tissue, which should not 
exist there, shows that the embryonal structure has failed 
to develop, as it should have done, into nerve elements, 



iS2 A CASE OF SYRINGOMYELIA. 

and, probably, most of these cavities are due to its disin- 
tegration. But a cavity in the posterior horn, or inter- 
mediate grey matter, may end at the middle line, by a 
rounded space in the position of the canal, and here an 
epithelial lining may prove that the cavity is continuous 
with the enlarged canal. I show you such a specimen. 
You ma}- remember that, at first, before the posterior com- 
missure is formed, there is a short extension of the canal 
on each side. It would seem that such cavities have arisen 
by the extension of one of these processes, after the union 
behind. 

But not only does the persistent embryonal tissue remain 
in the amount which we should expect from arrested trans- 
formation, — it is sometimes in much greater amount, and 
has manifestly been increased by a process of active growth. 
You may perceive indications of that in one of the sections 
under the microscope, in which there are rounded projec- 
tions into a cavity, clearly due to arrested development. 
The process of growth may much increase the quantity of 
this tissue, and even make it preponderate sometimes in an 
extreme degree over the cavity. A cavity may even 
become obliterated, perhaps quite early in life, by the exu- 
berant hyperplasia, and a state of " central gliomatosis " 
may effect damage, and cause symptoms, like those that 
are produced by a distended cavity. The cavities formed 
by these processes, and likewise the overgrowth of tissue, 
are most common in the cervical region; sometimes, how- 
ever, they extend a long way down the cord, and they may 
occasionally be seen in the lumbar region. The distension 
of the canal may also pass up even to the fourth ventricle, 
which may be increased in size, and the process of growth 
of the residual tissue may invade the floor of the fourth 
ventricle, and extend even as far as the upper part of the 
pons. Finally, as an additional evidence of the develop- 
mental and coneenital nature of the changes we have con- 



LOSS OF PAINFUL AND THERMIC SENSATIONS. 183 

sidered, it is not rare to find, in conjunction with it, some 
developmental defect in the brain. 

A few other forms of cavity are met with in the spinal 
cord, in rare cases, with which we need not concern our- 
selves just now. There may be a rarefaction of the grey 
substance, and a disintegration of it at some point ; but such 
cases are quite distinct from those which form our subject 
to-day. They are chiefly senile or due to manifestly 
acquired degeneration. I believe that a similar disintegra- 
tion of the white substance into a cavity only occurs in the 
neighbourhood of traces of undeveloped embryonal tissue. 
There, you may see that the nerve fibres and the interstitial 
tissue are alike scanty, and they may easily break down 
into an irregular cavity, the margins of which indicate its 
origin. 

You can readily understand that a morbid process which 
presents so many variations gives rise to symptoms that 
differ considerably in their character in different cases. In 
spite of these variations, in the great majority there is the 
loss of painful and thermic sensations. We do not yet 
know what mechanism in the morbid process gives rise 
to this peculiar symptom ; how far it is due to simple com- 
pression of the conducting tracts that convey these forms 
of sensibility, or how far it is due to damage to the fibres 
of the posterior commissure, by which we must assume 
that these sensory impressions cross. Again, when there 
is a cavity in the posterior horn, we can hardly conceive 
that the nerve cells, to which probably the nerve fibres first 
convey these sensory impulses, are not also damaged. 
These facts render it mysterious how sensibility to touch 
can so frequently escape. There are cases, however, in 
which all forms of sensibility have been affected. The 
affection of sensibility is commonly met with in the arms 
and parts of the trunk, very seldom, as in this patient, in 
the leg, though the legs are not seldom weak and present 



iS4 A CASE OF SYRINGOMYELIA. 

the characteristics of spastic paraplegia, a fact which we 
can understand when we consider the pressure which the 
pyramidal tracts must undergo when there is great disten- 
sion, or overgrowth of the embryonal tissue, or cavities in 
the lateral columns themselves. Muscular wasting, such 
as we see in this patient, is common, in one or both hands, 
sometimes chiefly in the shoulder muscles. It is appar- 
ently due to the damage to the anterior cornua by the 
enlarging cavities or compressing growth, and on the 
locality* of these its position depends. Other trophic 
changes are sometimes met with, the most frequent of 
which are lividity at the extremities of the hands, and inter- 
ference with the growth of the nails ; occasionally, especi- 
ally where there is muscular wasting in the upper part of 
the arms, there may be changes in the joints, especially in 
the shoulder and elbow, resembling those of tabes, and 
differing from those in chronic rheumatoid arthritis by 
the fact that the thickening takes place chiefly outside the 
capsule of the joint and not within it. Other symptoms, 
which, however, are rather rare, are the occurrence of 
ulcers and other changes in the nutrition of the skin of 
the fingers. More frequent are those which are due to the 
ascension of the affection to the medulla. The sympathetic 
may be involved by the lesion, so far as concerns the eyes, 
when the mischief extends to the upper cervical region of 
the cord ; and hence changes of the pupil-contraction have 
been sometimes noticed. The bulbar nerves occasionally 
suffer, and also those for the external ocular muscles, the 
nuclei of which may be reached by the distending force. 
In this patient there is weakness of the external recti, pro- 
bably due to the distension of the fourth ventricle. There 
is also nystagmus, which has the same significance, and is 
not at all rare in this disease. 

One other pathological fact should be mentioned to com- 
plete our general survey of the more salient features of this 



DEGENERATION OF PERIPHERAL NERVES. 1S5 

strange inalaay. In several rases a erenerati :r. has 'iter 
f:und ::: the peripheral cutaneous nerves. It has been 
zhiehy 1 coked :":r v.- hen there have been trtphic zhanves, 
and has tnen teen constant. It seems scarcery n.-te.y tnat 
the soeeial -ens : ry lass is due to this, since the ae venerate a 
nerves are of the extremities, and the loss of sensation is 
so extensive. 

Such a malady, so peculiar in its manifestations, is not 
lively:: ': e mistaken, prtvided :nly that its features are 
knew::. There are in been inly v: disease- vith v.-hich 
this is likely t: be :::::: u nded, provided you knov its fea- 
tures. One of these is chronic cervical pachymeningitis, 
in which there is much thickening of the cervical dura 
mater, and damage to the nerve roots. In such a case you 
have wasting and loss of sensibility in the arms, but the 
loss of sensibility involves all forms, is less ex:ensive. and 
is preceded by much pain. These are distinctions which 
seldom fail. The other condition is one which cannot be 
entirely separated from the disease we are considering, be- 
cause it seems to be, in part at least, due to the same morbid 
process; it is the affection which has become known under 
the name of " Morvan's Disease," or " Painless Whitlows." 
in which whitlows form on the fingers, and produce ulcers 
which do not heal for a long time, sometimes indeed only 
when the finger-ends have been lost. The pal nlessness is 
b::e t: thelzss :f sensibility t: z air.. :::::::: inly in ::::;:;:: :- 
ti in vith liss if sensibility t: tennaerature. : at ".nth::: t less 
t: teach. I n:ay nnentitn. as a striking instance cf the 
analgesia a:::n:aany:ng this affect! :::. that the shaalaer 
joint has been resected without pain, although : anaestheti : 
•as v:i 11 ; rvan's Disease " is f:ana :i be fee:: cavi- 
ties in the cord, similar to those in the condition of syringo- 
myelia, but combined, apparently in all typical cases, with 
extensive chronic degeneration, or degenerative neuritis, of 
the peripheral nerves. Its chief distinction is the presence 



1 86 A CASE OF SYRINGOMYELIA. 

of these painless whitlows, and there is usually a greater 
limitation of loss of sensibility to the lower portion of the 
limbs. This is thus rather a variety of syringomyelia than 
a separate disease. 

These, then, gentlemen, are the main features of syringo- 
myelia ; and the chief characteristics by which it is mani- 
fested. It is a disease for which, you will be prepared to 
hear, we are able to effect little by medicinal treatment, 
though we may be able to give temporary relief to its 
symptoms. This patient complained greatly, on his ad- 
mission, of distressing pain in the head, probably due to 
increased pressure within the cavities of the brain. This 
symptom has been greatly relieved by antipyrin. Elec- 
trical treatment may maintain for a time the nutrition of 
the muscles, but when their wasting depends on a morbid 
process that destroys the motor cells, we cannot hope for 
any regeneration of the nerves to reward our efforts ; we 
cannot anticipate any restoration of the path by which the 
will can act upon the muscles. But the future may per- 
haps have in store a ray of light to lessen the present 
practical gloom. Where the physician fears to tread, the 
surgeon sometimes steps in with the best results, and we 
must humbly bow in grateful recognition of the good he 
has succeeded in effecting in recent years, the lives he has 
saved, and the hindrance to the progress of disease which 
he has produced, the relief he has given, when we could 
not save or relieve or retard. But I am not aware that the 
surgeon's skill has yet been applied to this affection.* It 
seems to me that it is quite possible that, in some cases, 
surgery may be able at least to effect an improvement in 

* Since this lecture was delivered I have found a report of one case that 
was operated on in the manner suggested, without ill effects, with transient 
amelioration, but no permanent benefit. The case was, however, unfavourable, 
because the chief symptoms were in the legs, and cystitis ultimately caused 
death. (Abbe and Coley, Journ. Nervous and Mental Dis., July, 1882.) 



PROGNOSIS UNPROMISING. 187 

the condition of the patient, and a retardation of the pro- 
gress of the affection. The exposure of the cord would 
readily enable him to ascertain whether the process was the 
distension of a cavity by liquid, or the presence of a morbid 
growth. A central growth, extending high and low, 
could not be touched, but it may prove to be different 
when the chief element in the lesion is a distended cavity. 
The draining away of the fluid contents might enable a 
cavity to contract, and when the amount of circumferential 
growth is not too large, the relief from the slow compres- 
sion of the adjacent structures, would probably permit their 
recovery to a considerable extent, because no effects pass 
away so readily as those which are produced by slow com- 
pression, when that compression has been removed. 

The malady we have been considering is thus one of 
those developmental diseases on which we, as practitioners, 
can only look with feelings which are the reverse of grati- 
fying. It must be so. Such affections are the result of 
morbid tendencies, perhaps inherent in the germ, certainly 
beginning in the embryo, continuing in childhood, and be- 
coming active and aggressive in a later period of life. Their 
activity seems often to coincide with the completion of the 
process of growth ; but over the morbid tendency we are 
as powerless as we are over growth itself, or as the monarch 
of old was over the waves of the advancing tide. The ad- 
vance of these diseases is sometimes rapid, sometimes slow; 
sometimes, like the waves on the shore, they may seem for 
a time to give no evidence of onward progress ; they may 
even seem to recede, but it is only for a time. Before long 
a fresh advance carries their effects beyond the highest 
point they had before attained. But here, alas, we find that 
our simile fails us. The tendency of these diseases knows 
no retrocession. It is a tide which flows, but never ebbs. 



LECTURE XIII. 
THE TREATMENT OF MUSCULAR CONTRACTION. 

Gentlemen : — You are familiar with the fact that conse- 
quences of disease are sometimes more serious than the 
maladies from which they result. I do not now refer to 
the cases in which one definite disease is produced by 
another, such as the paralysis due to the poison that is the 
result of diphtheria, which causes such grave after-effects. 
I desire to draw your attention only to some simple results 
of disease, results that are the necessary consequences of 
the primary affection, — which we may almost describe as 
the natural effects of unnatural states. But, although they 
are normal consequences of abnormal conditions, they 
reach, by their simple increase, a degree which constitutes 
so definite a disorder that we are inclined to regard it as a 
morbid process. A morbid process it is, so far as its effect 
is concerned, although it is not a morbid process in its 
nature. It is disease only because it is an excess — because, 
in the absence of the normal limitation, it passes on to a 
condition which disorders normal action. 

This being the nature of the contractions of which I am 
about to speak, I must point out to you their causes and 
mechanism, that you may understand them, and that you 
may discern their nature when you encounter them ; that 
you may know what they mean, and that you may know 
how to remove them — to remove them if it may be, to 
lessen them if they cannot vanish, and, above all, to antici- 
pate their occurrence, to discern the conditions in which 

The Clinical Journal, March 6, 1895. 
188 



TOXIC CONTRACTION IN ORGANIC DISEASE. 189 

they will develop and yet in which they need not develop, 
to prevent them in the strictest sense of the word — to come 
before them, to stand in their way, to obviate them. 

Such a secondary process, arising from the unrestrained 
action of processes which are normal, is the cause of many 
of the results of disease which are most difficult to remove. 
Indeed, removal is only possible when the normal restraint 
can be renewed. The process of diminution even then is 
very slow. The renewal of restraint is gradual, and has to 
act on a tendency that has become far greater than normal, 
and, moreover, has a tendency to increase. This has first 
to be arrested before diminution of the abnormal degree 
can be achieved, and the normal restraint re-established, if 
its recover}- is adequate. 

I use these general terms because the conditions de- 
scribed, and the influences referred to of restraint on the 
one hand, and excess on the other, may be perceived in 
many morbid states, and their discernment enables us to 
understand better many processes and many consequences 
which outlive their causes. They often seem like indepen- 
dent maladies when they are only properly to be regarded 
as runaway vitality. For they depend really on the normal 
power of living structures to adapt themselves, by their 
nutrition, to conditions different in character or only in 
degree from those of health. 

This process, as I say, may be met with in many affec- 
tions, but in none more clearly than in the condition to 
which I want to direct your attention to-day, the muscular 
contraction met with in many paralysing maladies of the 
spinal cord and of the nerves. 

The tonic contraction of muscles that occurs in organic 
disease may be divided into two chief forms, easily distin- 
guishable, and important in their significance — that which 
yields to an attempt to extend the muscle, and that which 
cannot be overcome. 



r 9 o THE TREATMENT OF MUSCULAR CONTRACTION. 

I propose to consider to-day only the form that cannot 
be overcome. The calf muscles are often thus contracted 
as I show you in this patient, who is recovering from mul- 
tiple neuritis. When the foot is pressed up by the hand, 
placed against the sole, the calf muscles resist, the contrac- 
tion yields a little, and the foot is brought almost or quite 
to a right angle with the leg ; but however long you con- 
tinue the pressure the foot goes no further. That is the 
contraction which depends upon tissue-changes in the 
muscle, causing it to be structurally shorter than normal. 
It is of very great practical importance. You may remem- 
ber observing it in the boy with idiopathic muscular 
atrophy whom we examined last week. The first point 
for us to consider is to what it is due. 

It is met with especially in muscles that are less para- 
lyzed than their opponents, and is most common in the 
calf muscles, which extend the ankle joint, when the flexors 
in the front of the leg are paralysed. But we also meet 
with it when both sets of muscles are paralysed, and also 
in cases in which there is no paralysis, provided extension 
of the foot on the leg has been maintained for a long time. 
It occurs also in the flexors of the hip and of the knee if, 
from any cause, the patient lies in bed for a long time with 
these joints flexed. If you scrutinise the conditions in 
which it is met with, you will find that it is due especially 
to posture — that even paralysis is only effectual by induc- 
ing a certain posture. You know that there is an extraor- 
dinary capacity of the muscles to adapt themselves to pos- 
ture. Whatever the position of a limb or joint, the muscles 
must always continue in a certain state of slight gentle 
tonic contraction — "physiological tonus" or " tone " as it 
is called. If a limb is moved passively, the muscles which 
are relaxed do not wrinkle up ; they remain contracted in 
exact proportion to the approximation of their attachments, 
and the muscles which are extended elongate, but remain 



CONTRACTION OF THE CALF MUSCLES. 191 

in similar tonic contraction in exact proportion to the in- 
creased distance between their attachments. That capacity 
for adaptation to posture is evidently one phase of the 
condition which physiologists call " tone," and which de- 
pends upon the connection of the muscles with the spinal 
cord. From the nerve cells, in the anterior cornu, motor 
fibres proceed to the muscle. From the tissue between 
the muscular fibres, other nerve fibres pass up to the pos- 
terior cornu of the cord, and are connected, by a mysterious 
interlacement of fibrillar, with the branching processes of 
the cells of the anterior cornua. On the integrity of that 
arrangement this adaptation to posture and this muscular 
tone seem to depend. In consequence of that, if the attach- 
ments of a muscle are permanently and constantly approxi- 
mated in consequence of posture, the changes which, as 
you know, are always going on in every structure and 
every tissue of the body, alter the muscular fibres and the 
interstitial tissue, in accordance with the diminished length, 
so that after a time you are unable to extend the muscle — 
unable, that is, by any attempt which you may make at the 
time. We meet with this in cases of unequal paralysis, and 
also in cases in which one posture is constantly adopted. 
This effect of paralysis may be always traced to its influence 
in causing a certain position of the parts. That is the great 
cause of the various forms of talipes that result from the 
unequal palsy of muscles in infantile paralysis. The most 
common of these forms, that to which I want specially to 
draw your attention as typical of the others, is the contrac- 
tion of the calf muscles when those in front of the leg are 
paralysed. 

We meet with it also as the result of posture, determined 
by pain, and also of posture determined by simple comfort. 
It is probable that when there is infantile palsy with this 
sequel, the contracture of the muscles is facilitated by the 
fact that they also have suffered a little, that there are 



192 THE TREATMENT OF MUSCULAR CONTRACTION. 

slight interstitial changes, nuclear multiplication, with in- 
creased development of new fibrous tissue which contracts. 
But remember it is not a consequence of the palsy; it 
occurs without it — I mean it is not a consequence of the 
slight palsy of the contractor muscles ; it is the conse- 
quence of the persistence, for a long period, of the state 
that results from the capacity of the muscle for adaptation 
to posture. 

It is a grave inconvenience ; it hinders the recovery of 
use of the legs for standing and walking in patients who 
have otherwise gained sufficient power. It often needs 
division of tendons in order to permit the wrong posture to 
be rectified ; but it does not always need it. In many 
cases, unless there is shortening of the leg, the persistent, 
long-continued extension involved in the act of walking 
elongates the contracted muscle to its proper length. And 
that is the case in all conditions in which perfect recovery 
of the damaged structures causing paralysis is possible. 
It is conspicuous in adults — in whom no hindrance to 
growth can occur. In multiple neuritis, for instance, we 
have much greater palsy in the muscles in the front of the 
leg than in the sural muscles. The latter contract, in con- 
sequence of the posture permitted by the weakness of the 
flexors of the ankle. It is a disease which passes away 
under good conditions ; and however great that contrac- 
tion, it always in time yields to the attempt to stand and 
walk. Tenotomy is never needed. Tenotomy is only 
indispensable when the condition is due to a state from 
which recovery is impossible. In infantile paralysis it is 
frequently needed, because infantile spinal paralysis depends 
upon destruction of the grey matter of the cord ; recovery 
is impossible then, and without return of power in the 
opponents the contraction that results cannot be removed. 

But that which is difficult to remove may be prevented. 
The great cause of this contraction of the calf-muscles, 



A METHOD FOR PREVENTING CONTRACTION. 193 

permitted by the affection of the muscles in the front of the 
leg, is the action of gravitation in determining the posture 
of the foot as the patient lies. The foot " falls," i. e. f always 
sinks into a position of extension. The calf-muscles become 
shortened, first by active, extensible contraction, but this 
becomes fixed by nutritional changes, and ultimately is 
absolute by structural change. But the falling of the foot 
need not occur. It is a point of great practical importance, 
and is almost entirely neglected. There never need be this 
shortening of the calf-muscles from loss of power in the 
anterior tibial muscles. It is only necessary to keep the 
foot always up, and the contraction cannot occur. It may 
be kept up either by some support below the sole, such as 
a plank or a thick sandbag, or else by some traction of the 
foot. Support from below cannot, however, be maintained 
in adequate continuity. I have tried every form of support 
that could be devised, and have been compelled to fall back 
on traction. The force exerted need not be great ; a very 
gentle elastic traction, long continued, will keep the muscles 
adequately extended, and prevent the occurrence of this 
most troublesome result. But the contrivance of such 
traction is a much less simple matter than it may appear. 
There must be a place from which it is exerted. It must 
come from some part near the knee. However gentle it is, 
by long continuance it becomes annoying, then painful, and 
ultimately unbearable. It can be borne, indeed, for a very 
little time when there is tenderness, as there is always in 
the condition in which it is most needed — cases of multiple 
neuritis. I tried traction from the upper part of the bed- 
stead, but the changing posture of the patient made this 
useless. At last, after many trials of various forms, an 
idea occurred to me of a plan by which the traction could 
be exerted from the upper part of the leg near the knee, 
which has proved perfectly successful. I described what I 
desired to our excellent resident medical officer, Dr. Whit- 
17 



194 THE TREATMENT OF MUSCULAR CONTRACTION. 

ing, who speedily carried it out in perfect detail, with a suc- 
cess which is most gratifying. I show you here the apparatus. 
There is a leather sheath for the leg, almost meeting, 
laced together in front by a cord passing round the hooks. 
It may go above the knee or stop short of it. There is a 
similar sheath for the foot, and the two are connected by an 
isthmus of leather about an inch wide. From rings at the 




The upper figure represents the shape of the brown paper pattern, and 
of the leather, cut in correspondence with it. The dimensions are ap- 
proximate, varying with each leg. D is the narrowing for the knee, that 
the leather may not press on the bone at the sides. B is the excavation on 
each side for the ankle with the narrow connecting piece of leather, 
which is the special feature of the contrivance. This, I to I ^ inches 
wide, and no longer than is needful, affords, lengthwise, adequate support 
to make the pull from above act down on the foot-piece on which the 
pull acts. At H and G are the rings for the cords. The cords are here 
shewn only as going to the lower rings; if there is contraction of the 
knee they should be carried through these rings and fastened to the other 
rings above the knee. If there is no contraction of the knee it is not 
necessary for the leather to extend above the knee. 



end of each sheath cords extend, in which India rubber is 
interposed. A strong, common India rubber band answers 
perfectly well, for the elastic force, as I said, does not need 
to be great ; it needs only to be constant. The slightest 
constant traction is effective, but constancy, under varying 
mechanical conditions, can only be secured by elastic trac- 
tion. It is remarkable how well the muscles bear such 



UTILITY OF THE APPLIANCE. 195 

traction if only it is gentle. To the more sensitive skin it soon 
becomes unendurable, but the impressions from the afferent 
muscle nerves only act on consciousness, so as to cause 
" sensation," when excessive, and even long-continued 
gentle extension seldom causes muscular discomfort. 

The new feature which it embodies is this. The part of 
the apparatus for the \zgfrom which the traction is made 
is continuous with that for the foot on which the traction is 
made. The two are continuous by a narrow piece of the 
leather, which will bend so as to permit the traction to 
increase the flexion of the ankle, and so to overcome the 
shortening which has occurred, and which yet presents 
longitudinal resistance. This resistance is enough to make 
the source of traction, and that on which it is exerted, 
effectively one. Instead of the pull being from the leg 
itself, it is from the apparatus that the force acts on. Con- 
tinuous traction from the leg itself — which, however slight, 
becomes unendurable by persistence — is thus avoided. The 
traction is exerted from a part of the same structure as 
that on which it is exerted. This piece of leather, narrow 
and short as it is, affords sufficient support, and no pressure 
is caused on the leg itself. 

Another advantage of this apparatus is that it is easily 
made by any practitioner. A piece of leather must be cut 
out, of the shape which I now show you — two ovals con- 
nected by a narrow piece. It is best first to take a sheet of 
brown paper and cut out a pattern to fit the leg and foot of 
the patient. The leather must then be softened in water, 
warm at the last, so that the leather is warm when it is 
applied to the leg. It must be bound on the leg by cord 
or bandage, and then allowed slowly to dry and harden. 
The leg should be swathed to prevent chill from the drying. 
If thought desirable, oil silk may be placed next the skin. 
When dry and hard it is taken off. It has only to be lined 
with wash leather, and any shoemaker will insert in it the 



196 THE TREATMENT OF MUSCULAR CONTRACTION. 

necessary hooks and rings. A piece of cord and an elastic 
band complete it. It may be made in rough but perfect 
efficiency, with holes and tapes or cords, and a penny 
elastic band for traction. 

Mr. Hawksley, the well-known surgical instrument maker 
of Oxford Street, has made a copy of this apparatus, 
finished off with all due skill, and therefore more sightly 
than that which I show you, although it could not be more 
effective. He has been good enough to place it in his shop 
for any one to examine. As the only apparatus known to 
me that is really effective for preventing a grave evil, and 
even removing it when it has occurred, at least when it has 
not reached an extreme degree, and as one that is easy to 
make in perfectly serviceable form, I think it deserves to be 
widely known. It should be adopted in all cases in which 
a patient has to be kept in bed, and the weight of the foot 
leads to persistent extension of the ankle-joint, whatever be 
the cause of the condition, if there is the slightest evidence 
of commencing contraction of the extensors, or if there is 
even reason to suspect that it is likely to come on. 

But I have found that it produces another effect which I 
did not anticipate. When the leather is carried a little 
above the knee, as it is in the form shown in the figure, any 
tendency to flexion of the knee is counteracted, and with it 
flexion of the hip. When a disease that can be recovered 
from leads to such flexion, prevention is of great import- 
ance. When it occurs as the sequel to extensor spasm, 
treatment has little chance of doing good. The flexor 
spasm then says unequivocally, " Hope is at an end." 



LECTURE XIV 
THE INFANTILE CAUSES OF EPILEPSY. 

I. 

Gentlemen: — Many pleasant and useful memories remain 
to me of the two years' apprenticeship to a country surgeon 
by which I commenced the study of medicine. One inci- 
dent often comes to my mind in connection with the 
subject of infantile convulsions. I remember spending 
some hours in a cottage, one summer afternoon, watching 
a child in " teething fits.". The child was kept continuously 
in a warm bath. I do not know that my presence there 
was of much service to the patient, but it is of service to me 
now. It brings before me, very forcibly, the changes which 
have come to our conceptions in the thirty years that have 
elapsed. Fits, associated with dentition, were then always 
due to " cerebral congestion," excited by the irritation of 
the backward teeth, and it was necessary to keep the blood 
in the vessels of the skin that there might be less in the 
intracranial vessels. I remember well how the colour of 
the skin testified to the continuous action of the process, 
and yet how the convulsions continued without the slight- 
est alteration, although the " derivative " influence of the 
bath was so marked. It was, indeed, some years before 
this time that the true relation of convulsions to dentition 
was made clear by Sir William Jenner. But knowledge 
filtrates slowly through the profession, or at least its diffu- 
sion was then slow in rural districts, even among intelligent 

Clinical Journal, September 5, 1894. 
197 



198 THE INFANTILE CAUSES OF EPILEPSY. 

practitioners. The lectures on " Rickets " of Sir William 
Jenner not only marked, but made a turning-point in pro- 
fessional knowledge. The facts he demonstrated have now 
for long become general knowledge, and their chief source 
is lost to sight. The perusal of his lectures cannot, how- 
ever, be too strongly recommended, and, happily, their 
forthcoming reprint will make it easy. 

No one now dreams of associating the common convul- 
sions of retarded dentition with congestion of the brain, 
although a direct influence on the brain by the irritation of 
the process of teething is still sometimes thought to be the 
sole element in causation. In general, however, the influ- 
ence of the process of the eruption of the teeth is relegated 
to its proper place, as merely a possible excitant in a few 
cases. 

I hope it will not be very long before the progress of 
medical knowledge, and the improvement in medical edu- 
cation, makes " congestion " everywhere a morbid state that 
needs definite discernment, and not merely the equivalent 
for a negation. This may be, perhaps, too much to hope 
for. The assumption of " congestion " of this or that 
organ, of the liver in dyspepsia, or of the brain in hypo- 
chondriasis, is so easy ; its assertion is so precise, so satis- 
factory, and it enables treatment to produce such a definite 
result, that the assumption will not readily be regarded as 
a thing to be proved. As far as can be judged, its end is 
not yet. Of course, I am speaking only of the active con- 
gestion, which is constantly invoked to explain that which 
is not understood, not of the passive mechanical congestion, 
which is quite a different process, and is ignored when it 
exists as frequently as active congestion is assumed when 
it is absent. 

The service which Sir William Jenner did was to demon- 
strate that the condition of rickets is a general retardation 
of development, with various secondary, necessary results, 



DENTITION CONVULSIONS. 199 

and that the association of convulsions is with this general 
state, of which the backward teething is only one of the 
manifestations. 

The convulsions are a consequence of the retarded de- 
velopment which occurs so often towards the end of the first 
year. This epoch is one in which development is readily 
checked. Growth, indeed, goes on, but the progressive 
development of the tissues is hindered; their elements are 
still produced, but do not present the progressive develop- 
ment that should coincide with general growth. It is the 
epoch at which the character of the food-supply undergoes 
change, often unwise in suddenness, or does not undergo 
the change that is natural. It is a period also, when much 
functional capacity passes into functional use. Any general 
illness or prolonged digestive disturbance may have, as a 
result, distinct signs of this malady, but in considerable 
degree it is the result of preventible causes, which it would 
be foreign to my present purpose to discuss. 

The influence of rickets in causing such fits is of great 
importance in connection with epilepsy, because there is no 
doubt that such convulsions are a frequent element in the 
causation of that disorder. They leave behind a residual 
disposition to the like morbid action, which may be contin- 
uous in its results or may become active at a later period 
of life. Between the cases in which dentition convulsions 
have ceased after a few months and convulsions have 
recurred as epileptic fits at puberty, on the one hand, and, 
on the other, cases in which the infantile convulsions did 
not cease, but continued into life-long epilepsy, we have 
every gradation. There are cases in which the attacks 
went on for a few years, ceased for a year or two, and then 
returned, and cases in which the interval of freedom was 
five or six years. Indeed, every variation of interval is met 
with. It is thus impossible to doubt that the dentition con- 
vulsions are a definite element in the causation of epilepsy. 



200 THE INFANTILE CAUSES OF EPILEPSY. 

So constant, moreover, is their association with the defec- 
tive development which we call rickets, that it is impossible 
to doubt that the prevention of rickets would have a con- 
siderable influence in the prevention of epilepsy. 

One question to which I desire especially to direct your 
attention is this. How does the state of defective develop- 
ment cause the liability to convulsions ? I believe that 
they can be adequately explained by the simple fact of 
retarded development. This is conspicuous in all parts of 
the system. The morbid conditions that are characteristic 
of rickets can be, for the most part, explained by the per- 
version of nutrition, which is a necessary result of the 
retardation of the process. In the nervous system we 
know that, at birth, the state of the various structures 
differs, that some are structurally perfect, while in others a 
considerable amount of developmental change has still to 
occur before full functional capacity can exist. It is not 
necessary to describe the facts in detail, because the gen- 
eral character of the relation is alone important. The nerve 
structures which are lower in function, and in part in posi- 
tion, are developed before the higher. This is true of the 
motor elements and reflex centres. The lower centres are 
under the control of the higher, and their activity in early 
infancy, when the higher centres are less developed, is 
manifested in the restless, aimless movements of the child, 
and the conspicuous activity of the reflex processes. At 
birth these are developed to such a degree as to enable the 
mouth to suck, and the thorax and larynx to co-operate in 
producing too-familiar sounds. The process of develop- 
ment goes on, and as structure is complete, function be- 
comes established in more perfect degree. But the estab- 
lishment of perfect function follows structural completion, 
and it is long before the influence of the relative develop- 
ment ceases to have an influence on the action of the 
nervous system. Hence it is that all through infancy and 



DEFECTIVE DEVELOPMENT. 201 

early childhood reflex processes are so active. Their early 
predominance is only slowly reduced into subordination as 
the function of the higher centres becomes established in 
effective degree. It must be remembered that the motor 
centre in the cortex of the brain, from which impulses 
proceed directly to the spinal cord, is a centre relatively 
low, and its control by higher structure is a comparatively 
late event. Not only does this relativity of development 
and function explain the excessive spontaneous and reflex 
movement of infancy, but it explains to some extent the 
readiness with which the motor cortex acts in the sudden, 
violent manner which gives rise to convulsions. It is 
sudden and violent, although incomparably slighter than 
the convulsions of later life. It is important to remember 
the fact. Without doubt many of the attacks in infancy 
which consist only of tonic spasm, would in an adult con- 
sist of violent clonic spasm as well as of tonic spasm. The 
same activity in the well-developed centres for the larynx 
gives rise to the familiar " laryngismus stridulus." 

The hindrance to development, which acts upon all 
structures, of necessity has most effect upon those which 
are least complete. Where structure has become perfect, 
and function is established and is being fixed by use, its 
influence has little effect. Where structure is not yet 
perfect, and where it has just become perfect, but function 
is only just assuming its adequate form, the retardation has 
an influence in proportion to the imperfection of structural 
and functional development. It must be remembered 
that the retardation has an influence on growth and nutri- 
tion, and the effect on the finer nutrition which is related 
to function may be considerable, even after structural 
growth is at an end. Hence the relation of the lower cen- 
tres to the higher, the excessive activity of the lower, which 
is so conspicuous in early infancy, is reproduced by the 
influence of rickets. The excessive activity of early life, 
18 



202 THE INFANTILE CAUSES OF EPILEPSY. 

moreover, becomes definitely morbid insubordination. The 
greater capacity for functional action of the lower centres 
needs the proportioned control which should come from 
the due development of the higher, and this is wanting. 
Hence the uncontrolled activity is manifested by morbid 
action, possibly contributed to by the general failure of 
nutrition, which involves a less perfect form of action even 
in the centres in which development is complete and 
function established. Thus we can understand, without 
difficulty, the morbid action of the reflex centres which 
causes such a state as the contracture in the hands and feet 
and the laryngismus stridulus of rickets, and also the 
occurrence of the characteristic convulsions which prob- 
ably depend upon the lower cortical centres of the brain, 
those of the motor region. 

With the restoration of the normal process of develop- 
ment which comes from the treatment of the general state, 
the higher centres acquire increased control, and, in most 
cases, the tendency to convulsion ceases. But the sudden 
spontaneous overaction has left its residual effects. These 
may be so strong that there is no cessation of the fits, or 
only a brief cessation, or a recurrence under favourable 
conditions. Thus we have the series of cases to which I 
have already referred, which demonstrate the relation of 
such convulsions to ordinary epilepsy. The residual influ- 
ence, with its consequent tendency to persist or to recur, 
is certainly influenced by the mysterious functional state 
which is due to inheritance. The precise nature of this 
we do not know ; we can only guess it from its effects. It 
seems to be a defect in the chemical composition or the 
molecular structure of the nerve centres, in consequence 
of which nerve force is liable to be released without the 
stimulus which alone should excite this liberation. The 
tendency is seen in its special and isolated operation only 
after infancy is passed, but during this period it seems to 



INHERITED TENDENCY. 203 

co-operate with other conditions, and seems to increase the 
relative liability to convulsions in rickets. A slight degree 
of hindrance to development suffices then to give rise to 
the convulsions. Still more markedly does the inherited 
tendency dispose to the residual disposition to recurrence 
which is left behind by every fit, to which the persistence 
of convulsions is due, and still more again does it dispose 
to a recurrence, in consequence of this residual effect 
(which never entirely ceases) at some period in later child- 
hood or in youth. 

All parts share in the defective nutrition and in the hin- 
drance to their development. The bilateral symmetry of 
the frame involves the equal affection of both sides, and 
hence it is that the convulsions which are due to these 
causes are general. This is an important fact, as I shall 
hope to show in the next lecture. The persistent convul- 
sions which may earn.- on the malady from infancy to adult 
life are of the same general character. Often, indeed, the 
establishment of the control of the higher centres, when it 
does not arrest the process of discharge, modifies its form 
in a way we cannot yet understand, and attacks of " minor " 
character replace the convulsions, to be succeeded, at the 
time when epilepsy is most prone to develop, by convulsive 
attacks of greater severity. The convulsions of rickets, as 
I have said, in the slightness and tonic character of the 
spasm in a large number of cases, are nearer to minor than 
to major epilepsy. This fact is important because attacks 
of petit vial may succeed the convulsions of rickets and 
be unnoticed until spasm is again added. 

I need not say anything of the treatment of these con- 
vulsions, because it is well known to you all. But one 
point it may not be superfluous to mention. The bromide 
which is given to check the tendency to convulsions while 
the general treatment is re-establishing the proper course 
of development, should not be too hastily discontinued 



204 THE INFANTILE CAUSES OF EPILEPSY. 

when the fits cease. The residual tendency must be remem- 
bered, and this may be lessened, I believe, by continuing 
the treatment for some months after the attacks have 
ceased, and the time should be still longer when there is 
reason to think, from the fact of inheritance, that this ten- 
dency is likely to be profound. 



LECTURE XV. 
THE INFANTILE CAUSES OF EPILEPSY. 

II. 

Gentlemen: — The convulsions which we considered in 
the last lecture as a cause of epilepsy — those that occur 
during the period of dentition and are the result of the 
hindered development of rickets, are general. The later 
convulsions of epilepsy, which are developed from them, or 
disposed to by them, are also general. They are the char- 
acteristic convulsions of what is called " idiopathic " epi- 
lepsy. The convulsions of rickets are moderate in severity, 
and when they are continued into epilepsy, the attacks 
often become slighter, until they are merely minor attacks 
with loss of consciousness ; there may be only the slightest 
indication of spasm, or there may be no trace of spasm after 
a time. Such minor attacks may continue for a few years, 
and then again muscular contractions may be combined 
with the loss of consciousness ; increasing in severity, the 
seizures gradually assume the features of severe epileptic 
attacks. But the practical lesson to be learnt from the 
facts which we have considered is this : in a case of epilepsy 
which dates from convulsions in the period of the first den- 
tition, moderate in degree and general, whether the attacks 
have been continuous or interrupted by a few years' free- 
dom, you are justified in considering that the case is one of 
idiopathic epilepsy, founded on the convulsions of rickets. 

But there are two other forms of epilepsy in which the 

Clinical Journal, September 12, 1894. 
205 



206 THE INFANTILE CAUSES OF EPILEPSY. 

disease can be traced to infantile convulsions. The first of 
these is especially important. It differs from that we have 
considered in three features. The epileptic convulsion is 
one-sided, at any rate when moderate in degree, and if there 
is an aura, it is in one limb or in the face on one side. The 
spasm can generally be observed to commence locally in 
the hand or face. When both sides are convulsed, one is 
affected before the other, except in the most violent attacks. 
In these there may be no perceptible interval between the 
affection of the two sides. Inquiry regarding the character 
of the infantile convulsions will usually elicit the fact, when 
their character is known, that these also were confined to 
one side. The second feature is that the first attack of in- 
fantile convulsions was of great severity. Often, indeed, 
there was a series of convulsions, one after another, for 
several hours. Sometimes such a series was the only infan- 
tile attack ; often initial attacks were followed by others for 
a month or two, which ceased to recur when a few years 
had passed. Complete continuity of occurrence from in- 
fancy to adult life is less common in these than in the cases 
first considered. The third feature is that the first convul- 
sions often occur during some acute illness, or soon after a 
fall, or in a state of general physical prostration. This is 
not always the case, nor is it always true that there are 
several consecutive convulsions at the onset. But the first 
fit is seldom slight in degree, and, if the facts can be accu- 
rately ascertained, the first fits are known to have been 
unilateral. 

The unilateral character of the convulsion means uni- 
lateral instability of the motor structures of the brain. 
The commencement in one limb means local instability in 
a certain part of these motor structures. This part differs 
considerably from the rest in its morbid functional ten- 
dency. Such local change excludes a general cause, which 
would act on the whole brain. The suddenness of the 



ORGANIC DISEASE AT THE CORTEX. 207 

onset indicates a sudden development of the instability — 
that is, a sudden change at one spot. This is, however, 
equivalent to the assertion that the convulsions are due to 
a local lesion in the motor structures, because a sudden 
change means organic disease. Without doubt, this is the 
fact in the class of cases we are considering. There is 
organic disease at the cortex of the brain. Its occurrence 
is indicated by the initial convulsions. The effects of the 
process on the adjacent tissue, which is slightly changed, 
is such as to induce a permanent alteration in nutrition and 
function. In consequence of this, the structures "dis- 
charge " from time to time. The disease may be either in 
or only near the motor region. If it is in the motor region, 
and is more than minute, there is loss of power — hemi- 
plegia — the amount of which depends on the extent of the 
lesion. It may be such as to be persistent through life, or 
it may be transient and pass away in a few months. When 
the disease is only near the motor region, any initial loss 
of power may be too slight to be recognised. In an infant 
slight weakness on one side usually escapes recognition, 
and considerable paralysis may be unnoticed if the child is 
at the time prostrate from some general illness. When 
there is no lasting palsy, and when there is no history 
of initial palsy, we may nevertheless obtain some indica- 
tion of it. You are familiar with the aspect of cases 
of infantile hemiplegia, you know that they frequently 
present a peculiar inco-ordination of voluntary movement, 
especially conspicuous in the peculiar ataxy of the hand. 
When this is present in the arm, you will seldom fail to 
discern that in a slight smile there is more movement of 
the face on that side than on the other. You may often 
detect this when there is no other indication of hemiplegia. 
Corresponding to the side on which the convulsions begin, 
or to which they are limited, it is of very definite signifi- 
cance. Its significance, indeed, is far greater and more 



208 THE INFANTILE CAUSES OF EPILEPSY. 

trustworthy than you would conceive from the trifling 
nature of the symptom. It is only in a minority of these 
cases that we find persistent hemiplegia. The tendency to 
" discharge " in the motor structures is due to damage ; 
the hemiplegia is due to destruction. The tissues which 
are destroyed cannot give rise to convulsion. Hence, when 
the damage is too slight to cause persistent loss of power, 
or is situated outside the motor region but near it, so that 
the nerve elements in the motor region are damaged but 
not destroyed, the tendency to convulsions is met with in 
chief degree. 

The actual lesion in these cases is still a matter of con- 
jecture to an almost strange degree. Perhaps, however, it 
is not so strange. The lesion is comparatively slight, and 
vitality in early life is strong and has a marvellous power 
of resisting the influence of local disease, readily as it often 
yields to a general morbid state. Although the motto 
of the Pathological Society asserts that death is not 
silent, the truth is relative. Death has her secrets still, and, 
when death does not unfold the closed roll, the secrecy 
often baffles the most careful scrutiny. Not only is scrutiny 
baffled, but effort is tantalised, and the region of inference 
is a field of contest. Hence, opinions differ widely as to 
the character of such sudden lesions. Doubtless we shall 
not have to wait much longer before facts assist us. At 
present the opinion which seems to myself to deserve most 
weight is that there is a sudden occlusion of a small surface 
vein by clot, with the consequent intense congestion and 
hemorrhagic softening of the region of the cortex. In the 
softened region the nerve elements are destroyed ; an in- 
durated contracted area ultimately represents the disease. 
There is not usually the actual softening that is met with 
in arterial occlusion, or in traumatic injury, but on the 
margin of the chief destruction, in every form, there is a 
region of slighter damage, and it is, no doubt, from this 
that the discharges proceed. 



THE RESIDUAL DISPOSITION. 209 

Remember that the function of the motor nerve struc- 
tures depends on their ability to release a considerable 
amount of nerve force, without any appreciable interval of 
time after the stimulus reaches them. There must be a 
large amount of "latent energy" in the structures, which 
the stimulus at once releases as active force. In the struc- 
tures in which the nutrition is deranged by the previous 
process, the energy is not retained in its latent form until 
the proper stimulus releases it; it accumulates and escapes 
without any influence, that we can recognise, acting upon 
the structures to cause the release of the force. This we 
call " discharge." The process, once set up, spreads widely 
in proportion to its energy. If this is slight, it is limited 
to the part in which it began; if greater, it spreads through 
that side of the brain ; if greater still, to the opposite 
hemisphere. And note this — wherever it occurs, wher- 
ever it spreads — in every place the discharge leaves behind 
it a residual state disposing to its repetition. This resid- 
ual disposition is, in health, the foundation of all our habits, 
of all our education, of all our acquirements, muscular and 
mental. It is the physical basis of memory, and it is the 
basis of such functional disease as that which we are now 
considering. It facilitates the spread of the discharge, so 
that the convulsions after a time, become general more 
readily than at first. Remember this, because we shall 
presently see that it has an important practical application. 

Lastly, there is yet a third class of cases in which epi- 
lepsy has its origin in infancy. There are cases in which 
the first symptoms can be traced back, not only to infancy 
but through infancy — back to the earliest period of sepa- 
rate existence. They are cases in which there were con- 
vulsions during the first two or three days of life, or, at 
least, convulsive twitchings and other indications, such as 
difficulty of swallowing, of grave impairment of the brain. 
These cases occur in the children who are the " first-born," 



210 THE INFANTILE CAUSES 7 EPELEPS* 

who enter the world with greater difficult than those which 
follow them, and whose birth, as : can generally ascer- 
tain, was long and tedious, often needing the aid of instru- 
ments to terminate it soon enough to save the new life. 
You know that such children pass out of infancy into an 
imperfect physical childhood, with weakness of the legs, 
sometimes also of the arms, with irregularity* of the move- 
ments of the hands, and often also with convulsions. You 
have heard the cases described, and they have doubtless 
been pointed out to you as examples of the condition for 
which I have proposed the name of "birth-pals The 

symptoms are the result of damage to the cortex of the 
brain, commonly the effect of meningeal hemorrhage. 
When the damage is slight there may be no symptoms of 
paralysis, but its effect may be manifest by the occurrence 
of convulsions, either in childhood or in later life. Do not 
forget this because, although it is not common for epilepsy 
to be the sole effect, some cases, otherwise mysterious, can 
be thus explained. 

You will meet with fev. cases of epilepsy in which the 
fits can be traced back to infancy which do not fall into 
one of these three classes, and you will seldom have any 
difficulty in discerning to which class a given case belongs. 
Of the small remainder, most are associated with con- 
genital mental defect, and occur in families with neurotic 
disposition, and in which other instances of idiocy can be 
heard of. In these the malady must be ascribed to a 
congenital imperfection of the nerve tissue, of which the 
convulsions and the mental defect are both consequences. 
Such cases are usually self-evident In the others, those 
which I have considered in this and the last lecture, the 
diagnosis is determined by the character of the fits and of 
the initial convulsions, and the circumstances under which 
these occur. But there is one important effect of the in- 
fluence of attacks in disposing to their recurrence. A e 



IS OPERATION ADVISABLE 211 

long continuance of convulsions, which begin locally and 
spread to the other side, the spread becomes facilitated 
by the residual disposition, and its influence on the whole 
brain may be such that minor attacks occur quite like 
those of idiopathic epilepsy. They are typical attacks of 
the form which is understood by the term petit mal. You 
must not, therefore, let the occurrence of these have 
weight against other evidence that the original cause was 
a local lesion. 

A still more important question is connected with this 
residual disposition, and its action in augmenting the ten- 
dency to discharge of structures far away from the initial 
seat of the process. The question to which I refer, is that 
of the removal of the part from which the discharge pro- 
ceeds, the extreme instability of which is the source of each 
convulsion. The operation seems at first sight a promis- 
ing one, but the condition with which we have to deal 
differs much from the state in which there is some remov- 
able disease outside the nerve tissue, and acting upon it, 
such as depressed bone. Should the disease proceed 
from tissue which has recovered from partial damage, and 
which is in the vicinity :<f the original lesion, it is neces- 
sary to take away all that is around the latter in order to 
afford a reasonable prospect of the cessation of the fits. 
This involves, however, an increased loss of substance in 
the motor region, and an increased loss of function. 
There is at once increased loss of power, and although 
this lessens, it is permanently greater than before. It is, 
however, seldom sufficient to be put against the entire 
arrest of frequent and severe convulsions. Unfortunately, 
in a considerable proportion of the cases this arrest is not 
obtained. After an interval of freedom, which ex:::ts 
hope, the attacks return. This is not, indeed, surprising. 
The operation is only undertaken after long years of re- 
curring fits. Ever}- discharge has helped to fix the ten- 



212 THE INFANTILE CAUSES OF EPILEPSY. 

dency in the structures, and in greater degree the nearer 
they are to the original lesion. The operation itself can- 
not but have, on the adjacent structures, some of the 
influence which the original lesion had on those near it, 
and this fresh influence will be exerted on structures 
already accustomed to discharge. How profound the 
effect on the whole brain is in these cases, is sufficiently 
shown by the occasional occurrence of the minor attacks 
already spoken of. When the prospect of failure is added 
to the definite risk of the operation, which involves at 
least some danger that life may be terminated in forty- 
eight hours by acute cerebritis, its value must have been 
already reduced almost to zero by the fits to make the 
proceeding justifiable. 

Underlying all the phenomena of epilepsy, whatever its 
cause and whatever its features, there is one fact which it 
is important to recognise and to realise. Convulsions are 
far nearer normal action than their startling aspect sug- 
gests. In health, the nerve centres are always ready for 
the instant vigorous liberation of nerve force. A percep- 
tion of danger induces in an animal, and often also in man, 
motor activity as intense as that of an epileptic fit. The 
nerve structures, by their nutritional state, hold, ever 
ready for release, the latent energy which excites the mus- 
cles, and this in what we consider vast amount. Con- 
sidered from the dynamical point of view, it is no doubt 
trifling, not to be measured by its manifestation in the 
muscular contraction it excites. But the perfect readiness, 
which underlies its instant release in health, underlies also 
its instant liberation in disease, and thus it is less difficult 
for us to conceive the fact that the apparent causes of 
epilepsy are often such as seem to us inadequate. 

I have no practical facts of prognosis or treatment to 
state to you, which result from the causal conditions I 
have described, except this. The cases in which we can 



CONDITIONS OF PROGNOSIS. 213 

trace an organic cause are less amenable to treatment 
than are those which are purely idiopathic. When the 
infantile convulsions of rickets are the remote cause of 
the disease, the prognosis is only influenced by the long 
duration of the malady. But when an old organic lesion 
gives rise to the affection, and is perpetuated by its exten- 
sive influence on the functional action of the motor 
structures, the treatment which is useful in the idiopathic 
affection is less effectual. Exceptions there are, and most 
cases are susceptible of benefit, but on the whole we can 
feel less hopeful of effecting great good in such cases than 
in others. 



LECTURE XVI. 
NEURALGIA. 

To-day, gentlemen, I propose to ask your attention to a 
disease that you are certain to meet with, and certain to 
find among the most formidable, the most difficult, and 
even the most distressing of the practical problems with 
which you have to deal. The patient before you is suffer- 
ing from senile neuralgia of the fifth nerve. 

The mystery of pain presses upon our life on every side. 
It presses upon us in all our work, in every branch, but 
nowhere in such pure intensity and penetrating character 
does it tax our energy and baffle our resources as in that 
which is called the disease of pain, " neuralgia," " nerve- 
pain," because, in its special form, the pain is associated 
with some single nerve, as is that which is before us to-day. 
The prefix u nerve " refers to the limitation of the pain, 
and the name indicates the real character of the malady as 
a pure disease of pain. 

The part which pain plays in life is varied, but for it we 
should be, on the whole, thankful. Pain is essentially a 
warning of that which is worse than itself. It is a warning 
which incites escape from the coming evil of which it is 
the shadow thrown before. Without pain no life could 
long endure. Without the warning which pain gives, 
various influences by which life would be ended could not 
be perceived in time for its preservation. The great office 
of the sensory nerves which the human and animal frames 
possess in such abundance is to give indication of that 

Post-graduate Lecture, International Medical Magazine, March, 1895. 

214 



OFFICE OF THE SENSORY NERVES. 215 

which is external to the organism. It is to permit the 
outer world to act upon the nervous system, and through 
the nervous system to enable the organism to act upon the 
outer world. Through the sensory nerves all knowledge 
comes ; through the sensory nerves all guidance is afforded, 
and through them all warning of evil is obtained. The 
great agency of warning is pain. Without pain, without 
that which is incongruous, unpleasant in various degree, 
from the slightest discord to the intensity of asronv, there 
could be no adequate escape from that which is injurious. 

Yet it is scarcely correct to describe the influence of the 
external world as influence exerted through the sensory 
nerves. The accurate phrase would be that it is exerted 
through the afferent nerves, through the nerves which con- 
duct impressions to the central organs and by the agency 
of the central organs exert adequate effects upon other 
structures. We are sensitive, sensitive enough. We have 
more than enough of the impressions which acting upon 
and through our nerves reach consciousness. We may be 
thankful that there are no more. But, as a fact, it is prob- 
able that the afferent impressions which act upon conscious- 
ness are not more than one-tenth of the total amount of 
impressions which act upon the centres. Consider for a 
moment, as I have more than once asked students to do, 
how much of which we are unconscious we may become 
conscious of. Consider at this moment how from any part 
of your frame you may become conscious of sensory im- 
pressions which before you were wholly unaware of. I 
have sometimes asked a class of students to hx attention 
upon the vertex of the skull and note if they did not 
observe a distinct sense of pressure there, and I have been 
invariably successful in the result. I confess, however, it 
has been at the end of mv lecture, and not at the beginning. 
Therefore I am doubtful whether, at this moment, the effect 
will be sufficiently definite to justify my request. But the 



2i 6 NEURALGIA. 

impressions of which we may become conscious by atten- 
tion are but a small proportion of those which are forever 
passing to the central structures from every part of the 
frame, and the reality of this is shown by the fact that when 
intensified they are perceived as pain. 

Consider the significance of the pain of pleurisy, of peri- 
tonitis, of inflammation of the serous membranes. There 
is agony most intense, spontaneous, and produced by the 
slightest mechanical stimulus. The path for those sensa- 
tions must exist, and must be always a path of actual im- 
pressions, although they never reach our consciousness in 
normal states. This reserve, as it may be termed, of capa- 
city for pain seems true of even- structure, and everywhere 
we must conceive its significance to be the same, — that im- 
pressions in health are forever passing along the afferent 
nerves, impressions produced by varied processes of move- 
ment in the blood-vessels and perhaps the processes of 
nutrition, but impressions also which have their reflex influ- 
ence in guiding the other subsequent processes (as from the 
muscles) related to those from which they result, but which 
never reach our consciousness. Yet there we have the 
faculty, the capacity for pain, as an ever-present potentiality 
in every structure and in every tissue, in general a safe- 
guard against harm, harm of disease or harm of injury, — 
and in disease demanding, with a voice that cannot be un- 
heard, the needed rest. Yet this, by morbid action, may 
be developed to a disaster. The excessive development of 
the higher functions of the nervous system, which comes 
with civilized life, must, it would seem, entail an excess of 
the guarding capacity for pain. Consider the influence, 
through generation after generation without number, of an 
existence which we cannot conceive as really natural, at 
least if we look at the life of the red Indians, or of other 
races whose habits conform to the general relations of their 
organism. Civilized life, that is, a mode of existence quite 



FUNCTIONS OF THE FIFTH NERVE. 217 

out of harmony with our animal frames, must entail dis- 
proportionate development and elaboration of the parts of 
::n on which it specially acts. It must, of neces- 
sity, develop this danger-signal of pain into a degree of 
intensity and readiness of excitation which makes it at last 
one of the grave evils of life. 

Of that result we have the most conspicuous instance in 
neuralgia of the fifth nerve. This, surely, is natural. Con- 
sider what the fifth nerve is. I have alluded to pain a? a 
warning, a mode of guardianship. Guardianship is needed 
in proportion to the preciousness of that which has to be 
erved. The capacity for guardianship is proportioned 
to the readiness with which warning is produced, and to the 
effective degree which it readily attains. When we con- 
sider what the fifth nerve is and what it has in its charge, 
can we wonder that in this we have sensitiveness to pain 
d to the utmost degree and developed to the poten- 
tiality of disease ? Within its charge are the chief organs 
of special sense : the organ of sight, with all its marvellous 
delicacy of structure ; the organ of hearing, hardly less 
elaborate ; the organ of smell, with its relation to the en- 
trance of air; and, lastly, not only is the organ of taste 
within the charge of the nerve, but the nerve-fibres of the 
fifth nerve, so far as its root is concerned, are actually the 
channel by which impressions of taste reach the brain. The 
nerve has thus in its care the chief avenues for knowledge, 
and it has also within its guardianship the avenues by which 
matter, and all the energy that matter bears, enter the 
tern, — the opening of the alimentary canal and of the 
air-passages by which the oxygen passes to the system 
without which the food could have no influence. It is the 
guardian, as it were, of the gates through which enters that 
on which life depends and by which its power is supplied. 
It is, therefore, no matter of surprise that its functions 
19 



21 8 NEURALGIA. 

should reach a perfection, a capacity, which render it above 
all other nerves prone to disorder. 

In considering pain as a symptom of disease it is impor- 
tant to remember how much all our conceptions are colored, 
and how their form is determined, by our sensations. 
Consider the absolute distinction which we make between 
light and heat. We think of them as totally different 
things ; and yet it is a fact that the undulations of light in 
the red end of the spectrum which are perceived by the 
eye as red light are absolutely the same as those which are 
felt by the skin as heat. It is not that the heat and light 
coexist at the red end of the spectrum : they are the same. 
We give them different names simply because we have 
structures that respond to them in different parts and of 
different characters. As our sensations seem to us so dif- 
ferent, the causes of the sensations seem to us utterly 
unlike. 

That which is true of kind is often true of degree. As 
we regard the same influence as different because its effects 
are different, so we regard influences as great or small as 
their effect on us is considerable or slight. There is no 
necessary proportion between the intensity of pain and the 
degree of the impulse which causes it. There seem to be 
special nerves through which pain is normally produced, 
which we call "nerves of common sensation." But there 
is evidence that by many other nerves pain may be caused, 
if the impulse which when in moderate degree gives rise to 
another sensation reaches an intense degree. In the nerves 
of " common sensation," the nerves of pain, a most intense 
sensation may be produced by a trifling influence. Con- 
ceive what may be taken perhaps as a minimum of nerve- 
impulse, the instance which I gave in a recently published 
address, the lightest touch of a hair upon the skin. Con- 
ceive the actual amount of energy constituted by the nerve- 
impulse to which that gives rise, which nevertheless passes 



ORGANIC LESIONS OBSCURE. 219 

up to the brain and produces its definite effect. As I have 
said, to conceive it you must attenuate your ideas of 
energy to atoms. In the nerves of pain it is probable that 
intense pain may be produced by a nerve-impulse scarcely 
greater in actual dynamical amount. It is important to 
realize this, because it enables you to understand why the 
morbid process to which neuralgia is due should so often 
escape detection, should, indeed, be beyond our present dis- 
cernment. We have another illustration of it in the neu- 
ralgic pains of tabes. In a case of absolutely stationary 
tabes, with degenerative changes of the peripheral parts of 
the sensory nerves, there may occur from time to time, 
through years, paroxysms of agonizing intensity, and yet 
through all those years, with these attacks of pain coming 
and going, there is, as far as every other evidence can show, 
not the slightest increase in the disease. The changes in 
the extremities of the sensory nerves suffice to cause in- 
tense pain from the impulses which pass upward, impulses 
which may be an intensification of such as should be un- 
perceived or may be produced de novo. How slight may 
be the difference in the character of the impulse which 
passes up unfelt or causes pain may be shown by this, that 
a mere change in the weather will cause an attack of intense 
pain. 

As a matter of fact, in most cases of neuralgia of the 
fifth nerve, such as that which I am about to show you, no 
organic lesion has been found. It is a matter which is still 
uncertain. Facts can come but slowly to tell us whether 
most cases of persistent neuralgia of the fifth nerve are due 
to a peripheral or a central cause. It is most difficult to 
discern evidence one way or the other from the symptoms 
themselves. Among the facts that we have learned which 
seem of clear significance, there is the fact that disease of 
the centre of the fifth, in the pons, may give rise to such 
pain, that disease of the fibres in their course, perhaps also 



22o NEURALGIA. 

in the Gasserian ganglion, may give rise to such pain, and 
that disease of the peripheral termination of the fibres may 
give rise to such pain. It is important, in connection with 
the conception of the pathology of neuralgia, to realise the 
fact that the nerve-fibres which conduct differ only in degree 
from the structures which generate the nerve-impulses. I 
have elsewhere laid great stress upon this fact. It has been 
brought out bv recent discoveries resrardincr the structure 
of the grey matter of the nervous system. These discov- 
eries have an important bearing upon almost every problem 
of disease. The nerve-fibres, those, for instance, of the fifth 
nerve which reach in the pons and disappear from percep- 
tion in the spongy substance of a long column of grey 
matter, probably end in that substance by terminations 
slightly thickened, it may be, but absolute. We used to 
say, we used to think, that the nerve-fibres end in the cells 
of the grey matter. The cogency of the facts which have 
been brought forward prevents me, for my own part, from 
entertaining any doubt of the correspondence of the new 
statements with fact. We must conceive that from the cells 
of the nucleus of the fifth nerve branching processes go off 
which end by contiguity', but not by continuity, with the 
ends of the fibres that conduct. We must conceive that 
the impulses which pass up leap in some way from one to 
the other. I say " leap," but it maybe that the most pow- 
erful microscope would not reveal the chasm over which 
they leap. Yet it is absolute ; a break in the molecular 
continuity which permits the passage of chemical action. 
The leap is probably by simple motion, like that which 
produced the impulse in the first instance at the periphery, 
where branching processes of the cells (that is, of the long 
fibres) end or begfin in sli^htlv enlarged terminations in the 
skin. 

I spoke of " branching processes," but I should rather 
say " separated fibrils." I need not go into that distinc- 



COMPLEX STRUCTURE OF GREY SUBSTANCE. 221 

tion, although it is one of fundamental importance, because 
it is explained fully in an address I have lately published, 
and in which these facts and opinions are readily acces- 
sible to you.* Remember how extremely complex is the 
spongy structure of the grey substance in every nerve- 
nucleus ; that we have innumerable fibrils in close rela- 
tionship, and among these there must be terminations 
which constitute definite paths in the closest contiguity, 
so that impulses readily pass from the one to the other. 
Others must be sufficiently near for an energetic impulse 
to pass between them, but not for a slight impulse in the 
closest, and among these we can readily understand that 
there may be a difference in special excitability at the time. 
An impulse may even reach the centre and excite an adja- 
cent fibril ending more readily than the ending which is in 
strict relation to it, because the former is the more excit- 
able. If we conceive, as I think we must, that the nerve- 
impulse which begins by excitation from simple motion, 
which is propagated by chemical processes as a form of 
motion, may pass again as simple motion where the 
absence of continuity prevents the chemical transfer of its 
special form of motion, it is not difficult to understand that 
adjacent fibrils may be thus excited, and that we may have 
what is called an " irradiation of sensation." 

I remember a personal instance of that. Unpleasant as 
personal experience may be, never forget that the most 
useful knowledge of your professional life is that which is 
subjective. I remember having a carious tooth in the 
lower jaw, from which I suffered no pain. After a time I 
had an attack of recurring paroxysms of intense neuralgic 
pain in the upper jaw, just opposite the tooth, but never 
associated with any pain in the carious tooth. At last I 



* "The Dynamics of Life.' ; London: Churchills ; Philadelphia : Blakis- 
tons. 



222 NEURALGIA. 

had that tooth extracted. The process of extraction 
caused the most intense paroxysm of pain in the upper 
jaw that I had ever experienced, and — it was the last. 
There can be no doubt that the irritation of the inferior 
dental branch of the fifth nerve had in some way, probably 
by some increased susceptibility of contiguous fibrils, led to 
their special excitation, and their stimulation had reached 
a morbid degree, intensifying itself until it possessed the 
capacity for neuralgia. 

These new facts of the relation of the nerve-structures 
do enable us to understand many phenomena better; and 
that which explains much is seldom wrong. We can 
sometimes discern truth most surely by perceiving how 
much that is obscure is made clear, how much that is dis- 
cordant is brought into harmony, how much more we can 
look for than before could be conceived. 

Among the many varieties of neuralgia which you will 
find arrayed in text-books in serried ranks of formidable 
length and imposing order, three groups are specially 
important: (i) The neuralgic pains which occur at all 
periods of life from definite local irritation, such as that 
which decayed teeth induce. (2) The changing neuralgic 
pains that we meet with especially in middle life, — when a 
neuralgic pain comes in one part, then passes to another, 
then may leave and go to a third, then perhaps will change 
to some other temporary neurosis, and then may vanish as 
an altogether different malady comes on. (3) The class of 
which this case is an example, — senile neuralgia. 

Neuralgia in its intense severity and enduring form is a 
malady of late life. It is the most formidable, the most dis- 
tressing disease that life can bring, and it comes when the 
clouds should clear for the placid sunset, always longed 
for, seldom obtained. It is a disease of age. The influence 
of age on neuralgic pain is an important and significant 
fact, shown in a most striking way by the neuralgia which 



INFLUENCED BY AGE. 223 

follows herpes. After the age of fifty years post-herpetic 
neuralgia is prolonged in proportion to age, or rather its 
persistence is longer and far greater than the ratio to age. 
In middle age the neuralgia is trifling, and will last only 
for a week or two, but at seventy it will last for years, and 
may never pass away entirely. That is true irrespective of 
situation. I remember that Sir William Jenner used to tell 
us of one striking instance of this. A man had herpes zos- 
ter on the calf of the leg. It was characteristic, and had 
left the usual sequel. It was before the days of chloro- 
form ; he had everything done which could be thought of, 
and at last he consented to endure the pain of having that 
part of the skin and muscle cut away. Obtaining no relief, 
he shot himself. That may impress on you the intensity 
of the pain in the old which is trivial in the young. Why it 
should be I do not know, but we may form some dim con- 
jecture when we remember that all these nerve-impulses 
are matters of, as far as we can see, chemical processes 
occurring in the tissues under the influence of life. The 
vital power of nutrition is the influence which renews the 
capacity for function, by replacing the molecules which 
have been changed by the functional action which has just 
occurred. As life goes on, the capacity for renewal 
becomes less perfect, so that molecules are formed less 
competent to achieve their purpose, more prone to give 
rise to abnormal impulses, and recovery from any other 
morbid process produced by outside influences is less per- 
fect. The restoration of structure is not such as to enable 
it to do the normal work in perfect degree, and the degree 
of imperfection of constitution, so slight, it may be, as to 
us to be scarcely conceivable, may determine a morbid 
function adequate to produce intense pain where under 
normal condition hardly any sensation should be caused. 
Every morbid functional action is followed by a renewal of 
capacity for like action, but renewing it every time in an 



224 NEURALGIA. 

increased degree. The nutritional power of life is an aug- 
menting influence, potent for all acquisition of capacity, 
healthy and diseased. The disorders of the nervous sys- 
tem that depend on morbid action are, by the vital pro- 
cesses of nutrition, self-perpetuating. 

This patient is forty-seven years of age. Her case makes 
us call to mind as possibly important the fact that senility 
is individual, so far as concerns the time of life at which 
age becomes " old age," and come the transition must, 
unless the shears snap the thread before it breaks. It is 
not only individual, but often partial. Every grey or hair- 
less head reminds us of the fact, and should prepare us to 
meet with local troubles in some patients which are com- 
monly met with only in those who are much older. The 
patient is younger than most subjects of her malady. But 
in life's sad cadence, tones only just distinct in one genera- 
tion dominate that of the next. The patient inherits neu- 
ralgia, but not in its senile form. Her mother suffered 
from nerve-pain for several years, but in another seat and 
form. The transmission of tendencies to disease rather 
than of precise disease is forever rising conspicuously 
before us when we endeavour to discern the relations of 
the morbid processes we have to treat. Each tendency 
may be inherited in hindered or augmented form, often 
through causes that we cannot trace. Senile changes in 
one person may come only a little before due time, and in 
the offspring may be definitely premature. The strength 
of tissue vitality varies, and is capable of variation through 
direct and indirect influences. Its primary influence is on 
function, the changes in nutrition first thus manifesting 
their presence. Ultimately derangement increases to loss 
as nutritional alteration advances to structural change. 
But this is clearly seen only when function readily reveals 
the early change. 

There is another class of cases in which the inheritance 



ENTAILMENT OF DISEASE TENDENCY POSSIBLE. 225 

of disease depends upon the inheritance of structural pecu- 
liarities, unimportant in themselves, incapable of manifest- 
ing their presence, and yet determining in an adventitious 
manner grave disease. Thus early death may be inherited 
through that which, save for its position, would entail no 
difference in any one of life's many features. Yet a simple 
inherited peculiarity in anatomical arrangement may entail 
inherited disease. I remember a peculiarity in the retinal 
artery that was the same in mother and daughter. I can- 
not doubt that a like inheritance of arterial branching may 
determine strain on certain cerebral vessels, and early 
atheroma so situated as to entail occlusion of an important 
branch. So also we may conceive that in nerves inherited 
characters may determine definite effect, and that far more 
frequently, and far more powerfully, inherited tendencies to 
nutritional failure or nutritional susceptibility may induce 
functional disorder. It may be transient in middle life, but 
enduring when in later life the vital power fails to maintain 
adequate nutrition, — that is, the due appropriation to the 
molecules of the elements on which the proper action de- 
pends. We can understand that the liability to derangement 
at one age should be inherited as a liability to later failure, 
and that thus this woman should now present the most in- 
tense form of senile neuralgia, whose mother suffered from 
varying though severe neuralgia in other parts at an earlier 
time of life. It is four years since the pain, now so intense 
as to make her life one long agony, began. A decayed tooth 
was thought to be the cause of the pain. Many such irri- 
tative causes of neuralgia are real, although their removal 
may not cure, as with tapeworm and epilepsy. 

Epilepsy — i.e., repeated convulsions — may be due to tape- 
worm. It may be expelled, with its head, once and forever, 
but the fits go on, just as all the consequences of evil deeds 
live afterwards. 

Paroxysmal pain is the analogue of paroxysmal spasm. 



226 NEURALGIA. 

It is facilitated by repetition, as is every functional process 
by the residual effect of augmented capacity. In this patient, 
moreover, some constitutional condition of peculiar charac- 
ter may have been at work. An inherited disposition may 
be augmented by another. The patient had, during each 
pregnancy, neuralgic pains in one cheek. The influence 
of pregnancy is often definite, but seldom the same. This 
morning I saw a lady subject to intense migraine who 
never had an attack during pregnancy. The relation of 
the state of pregnancy to the nervous system is alike im- 
portant and mysterious. Why it should induce or hinder 
the same morbid state we do not know. We shall learn 
some day, and with it much more. The last attack in this 
patient began eight months ago, and has continued. It was 
sufficiently severe to cause the extraction of all her teeth. 
The pain persisted though the teeth were removed. Above 
the upper molars is, as you well know, a curious cavity 
called the antrum, a convenient receptacle for conceptions 
of disease. Her antrum was then opened, apparently with 
the object of permitting the escape of whatever disease it 
might contain. Whatever was released, the pain remained. 
The operation did no good. But morbid processes do not 
always avail themselves of the opportunities offered them. 
So then her antrum was drained. But the source of pain 
was not even drained away. Yet some effect resulted. She 
improved slowly. We should remember that many remedial 
measures which do not do good directly do harm indirectly 
by lessening the patient's strength. This is a rule appli- 
cable to many diseases, which is rather apt occasionally, in 
the flush of therapeutic energy, to be lost sight of. 

She is now suffering from many attacks every day, or 
was until she came here, and each begins by a curious 
sensation, which is not actual pain, near the junction of the 
left lower alveolar margin of the ramus of the jaw. She 
describes a flickering sensation at the extremity of the 



AUGMENTATION OF INHERITED TENDENCY. 227 

upper gum. This soon becomes a darting pain, which 
spreads to the lower jaw and seems to pass upwards and 
backwards. Sometimes it begins in the lower jaw. Any 
movement, any touch, will bring on a paroxysm, especially 
if it is a little time since she has had one. The attack 
seems in some way to exhaust the tendency, so that a 
touch immediately after an attack will not cause one, while 
the same touch would cause one after an interval. It is 
just as with migraine: a patient who, a month after an 
attack of migraine, could not eat a mince-pie without 
another attack, may eat two such evil but pleasant things 
a few days afterwards without effect. So also it is with 
epileptic attacks. The recurring influence of each func- 
tional process is to induce a nutritional development of 
renewed tendency, which takes some time to reach a high 
degree. Except just after an attack, any movement of her 
tongue in that part of the mouth will excite a paroxysm, 
but the more sudden the movement the more severe and 
immediate is the pain. I can show you the difference. 
You will see that a very slight touch, if sudden, will cause 
an attack of pain, but a very much more severe pressure 
may be made very gradually without pain. It is one in- 
stance of a general law. A galvanic current gradually 
increasing maybe passed through a nerve without exciting 
it, but if suddenly increased it at once causes stimulation. 
This is true also of the interruption of the current. I can 
show you a similar effect in the mechanical effect of pres- 
sure on the sensitive nerves of the patient. I press very 
gradually until at last I am pressing firmly, and yet the 
patient says that it does not produce pain. I press sud- 
denly, and you see at once evidence of suffering. I again 
press gradually, and gradually lessen the pressure, and 
there is no pain. Again I press gradually, and suddenly 
withdraw the finger, and pain is acute. The patient has 
had fewer attacks of pain during the past week, but she 



228 NEURALGIA. 

has had more slight continuous pain. The substitution of 
this for the intense paroxysms is probably an improvement, 
but the patient seldom realises it. A present evil, vivid in 
its experience, always seems greater that that which mem- 
ory only presents to the consciousness. The slighter con- 
stant pain seems to her harder to endure than even the 
frightful paroxysms she suffered with intervals between of 
perfect freedom. The patient has been admitted with a 
view to an operation upon the nerve, but at present we 
have only an example of the frequent difficulty that is due 
to some improvement produced by the perfect rest or by 
the treatment it is right to try. 

The result of division of the nerve is sometimes great 
and sometimes most disappointing. Benefit apparently 
depends upon the effect of preventing all afferent impulses 
from the periphery. When the neuralgia depends upon 
nutritional changes in the centre, rendering it unduly active, 
so as to generate impulses, the activity may be kept up, 
and the paroxysms of pain caused by impressions from the 
periphery which normally would have no effect. If the 
morbid process is actually in the periphery, or in the nerve- 
fibres which conduct and are also excitable, and the nerve 
can be divided above the morbid process, then the morbid 
impressions are arrested. But it may be that even then the 
effect is not absolute, because the repeated abnormal im- 
pulses giving rise to the pain may have brought the centre 
into a state of spontaneous over-action, and neuralgia, 
primarily peripheral, may be ultimately central, and thus 
continue when the peripheral cause is removed from action. 
It is a similar process to that of epilepsy due to a tapeworm 
in the intestine, and may persist for years after the cause is 
expelled. Such arrest of the peripheral impressions is a 
point of great importance in treatment, but it is so formid- 
able that only when other measures have failed can it be 
proposed. In many cases, especially in those which are 



THERAPEUTICS. 229 

not of long duration, we have the means of lessening the 
peripheral impressions for a little time each day by the 
hypodermic injection of cocaine, and, slight as this may 
seem to be, yet by its repetition it has often in time an 
unquestionable influence. Moreover, the importance of 
combining several influences, each of which alone has but 
slight effect, is often strongly impressed on the practitioner. 
It interferes seriously with the progress of therapeutic 
science, but we have to gather for the general good the 
fragments that we can secure without individual harm. 

I can glance at some only of the more important of the 
other general elements in treatment. Apart from the 
removal of causes and the operative treatment, the chief 
measure is the promotion of the general health by every 
means in our power, avoiding whatever lowers the tone of 
the nervous system, and endeavoring to strengthen it by 
drugs, and to lessen, if we can, the tendency to its over- 
action in the same way. I do not hesitate to speak of 
treatment by drugs. I hold that their influence is by con- 
veying energy in special forms to special structures in which 
energy is evolved. I wish we could associate drug with 
drag and draw. Alas ! Professor Skeat forbids, and from 
his decision there is no appeal. He only permits us, as 
the source of the word, dried roots and sugar-plums. Well, 
" these things are an allegory," without doubt, but not that 
which I desire. In passing, may I ask if you know Skeat's 
" Concise Etymological Dictionary," in which words are 
arranged according to their derivation ? If not, let me 
urge you to spend on it the first seven shillings and six- 
pence you can save or beg (I will not go farther, though I 
almost might). But, frankly, if a copy cost five pounds, I 
would sell any books I have, to that value, in order to 
obtain it. 

To see the real significance of the use of drugs — as 
dynamical therapeutics — we must realise that all the im- 



230 NEURALGIA. 

pulses in the nervous system are the result of chemical 
processes occurring in the nerve-tissue. In this the mole- 
cules, their composition and arrangement, are determined 
by the influence of life, mysterious, inscrutable to us, per- 
haps, forever. But the processes depend on energy latent 
in the molecules, released by chemical union. Most drugs, 
like most food, are of value, not as matter, but because they 
convey energy. These chemical compounds present latent 
chemical energy in certain forms, and by entering into the 
composition of various structures they modify their compo- 
sition or action or both : thus they do good ; thus also at 
times they do harm. But into this question, fascinating as 
it is, I cannot go. You will find its grounds discussed in 
the address I have already referred to. 

In the treatment of neuralgia I confess my own experi- 
ence does not lead me to express any high estimate of the 
older drugs, such as sulphate of copper, but the influence 
of direct sedatives is unquestionable. The influence of 
cocaine is purely local — it is simply to arrest the afferent 
impulse; but the influence of morphine is central — it has 
special action upon the sensory structures. A strange 
thing, which may not have struck you, is that morphine 
and opium seem to have a special action upon the centre 
which is over-acting, so that the agents will quell pain with- 
out producing sleep, and indeed at first in doses too small 
to cause sleep, if only they reach the centres with the 
sudden momentum secured by hypodermic injections. As 
a rule, in my observation the greatest benefit has been 
obtained from the milder sedatives, especially Indian hemp 
and gelsemium, while the tonic effect that is usually essen- 
tial for permanent benefit is produced, I think, even on the 
sensory structures, by strychnine more effectually than by 
any other drug. Its effect also seems to be proportioned 
to the momentum with which it is brought to bear upon 
the elements, and as it is not always convenient to give it 



TONIC SEDATION. 231 

as a hypodermic injection, and it is well to convey the mo- 
mentum of its tonic influence with the momentum of gentle 
sedative influence, I have been accustomed to combine 
strychnine with Indian hemp or gelsemium, and to secure 
their more rapid transit by giving at the same time nitro- 
glycerin. Ourpharmacopceial one-per-cent. alcoholic solu- 
tion called tinctura trinitrini is most convenient for the 
purpose. The important thing is that the initial dose 
should be uselessly small and rapidly increased, and that 
the mixture should not be alkaline. From this I have seen 
results, even in such cases as the patient before you, ex- 
ceeding anything I could have expected, giving greater and 
more permanent relief than any other therapeutic measures, 
so much so that the treatment has made it unnecessary to 
operate on some patients who were admitted for that 
express purpose. 



LECTURE X VII. 
LEAD PALSY. 

Gentlemen : — You remember the case of lead palsy, or 
wrist-drop, which I lately showed you. I wish to-day first 
to mention some practical points in connection with the 
affection, and then to point out to you the general aspect of 
the disease as it is revealed to us more clearly by the 
recent increase in our knowledge of such causes. 

The first practical point relates to diagnosis. The palsy 
is so generally connected with lead, that it is seldom mis- 
taken. The danger is lest other things should be mistaken 
for it. Yet the practitioner or student at once looks at the 
gums, and the lead line at once indicates to him that the 
cause which he expects is present. But it is important to 
be aware of the fact that this trust is only justified when 
the gums are not perfectly close to the teeth. A like palsy 
is the result of other poisons ; but in their case there is to 
be found no line upon the gums. Alcohol, arsenic, and 
perhaps other metallic poisons may cause the same palsy, 
but the absence of a line upon the gums excludes lead as 
a cause on that one condition — provided the gums are 
anywhere separated from the teeth by a space in which 
there are decomposing albuminous materials capable of 
yielding sulphur. With perfect gums you can only ex- 
clude lead-poisoning by excluding its possible causes, espe- 
cially by having the drinking water analysed, and by hav- 
ing the urine analysed after iodide of potassium has been 
taken for a week. 

Clinical Journal, May I, 1 895. 



DIFFICULTIES IN DIAGNOSIS. 233 

But the most difficult point in diagnosis, in my own 
experience, is due to this strange fact, that a chronic spinal 
muscular atrophy occasionally begins with rapid weakness 
of the extensors of the arms on both sides, having exactly 
the onset and the localisation of lead palsy. In the cases 
I refer to, of which I have seen several, this has been 
followed by spreading muscular atrophy elsewhere in the 
arms and trunk, and by other indications of morbid process 
in the spinal cord. In none of the cases was there a veri- 
fication. Yet I could entertain no doubt of the truth of the 
fact, especially as every toxic cause was excluded. In the 
early stage, when there was simply the rapid weakness, 
with degenerative reaction in the extensors of the forearms, 
precisely localised as that of lead poisoning, the diagnostic 
question was one of the most difficult that can be con- 
ceived. As soon as spreading atrophy was obvious else- 
where, the question became simple ; but it has happened 
that the difficulty was, at first, the greater in some cases I 
have seen, because the gums were so perfect that the 
absence of a lead-line was unimportant. Its absence had 
none of the significant meaning its presence would have 
afforded. In such cases you have only to wait and watch. 
In other cases of toxic origin you have, as a rule, sufficient 
evidence of the poison, from other symptoms, or there is 
weakness in the corresponding muscles of the legs which 
you know to be such a characteristic of alcoholic palsy, 
and is scarcely ever present in lead palsy. That is also 
the case with arsenic. Wrist-drop may result from arsenic 
precisely like the wrist-drop from lead, but there is also 
similar palsy in the homologous muscles of the lower leg — 
those which flex the ankle and extend the toes. I think I 
have mentioned to you an instance of that which came 
under my notice — a case of symmetrical palsy of the arms 
and legs in a lady who had been working for years on 
some muslins. They had been bought as possessing a 



234 LEAD PALSY. 

specially " aesthetic " colour. But a " thing of beauty " is 
not always a joy forever. The muslins were found to be 
charged with arsenic. The palsy lasted long, but recovery 
was ultimately completed. 

There is an interesting question which may sometimes 
be important to you with regard to the "lead line." You 
know that the treatment of lead-poisoning consists in giving 
iodide of potassium. And why? Iodide of lead is abso- 
lutely insoluble ; why, then, do you give iodide of potas- 
sium? For this reason, — and remember it as an instructive 
instance of the necessity for caution in letting theory deter- 
mine practice, — that, although iodide of lead is absolutely 
insoluble, by giving iodide of potassium you increase the 
quantity of lead in the urine. Here, then, is a practical fact 
on one side, and a theoretical fact on the other. I yield to 
no one in regard for theory, but theory is nowhere beside 
fact, and you do eliminate the lead by giving iodide of 
potassium. The fact is, that lead is in the system in com- 
bination with albuminous substances, and the iodide seems 
to form a combination with them that is soluble. The 
effect, therefore, of giving the iodide is to increase the ex- 
cretion of lead, and, of course, to do this it has to increase 
the amount in the blood. You have, therefore, to be a 
little careful, when much lead has been recently taken in. 
Before you give the iodide, you should clear out the lead 
from the alimentary canal by giving an aperient for a few 
days ; and then you must give but little iodide at first. 
That is the essential treatment. 

But the point I was going to mention is, Does the iodide 
remove the lead line from the gums ? The lead is in the 
form of sulphide of lead. We cannot a priori infer that the 
iodide will act on the sulphide of lead as it does on the lead 
in combination with organic substances. My own obser- 
vation has afforded me no instance in which the iodide of 
potassium has removed the lead line ; and I have seen cases 



SIGNIFICANCE OF THE LEAD LINE. 235 

in which, after the ingestion of lead had ceased for some 
years, the lead line was as perfect as ever, although iodide 
of potassium had been taken at the beginning for many 
months. This is not a theoretical question only. 

You may be in doubt whether given symptoms are due 
to lead in a patient who, say, a year before had certainly 
been exposed to the risk of lead poisoning, or had had lead 
poisoning, had been treated with iodide of potassium, and 
had gums such as would give rise to a lead line. Is the 
absence of the lead line of significance as regards the ques- 
tion whether present symptoms may be still due to lead ? 
May the lead line have been removed, and some lead be 
still elsewhere in the system ? I think not. I think that 
if lead still existed in the system there would certainly be 
a lead line. The point may come under your observation 
practically in more than one way. A case which brought 
it very prominently before my mind was that of a middle- 
aged man who had been gradually losing his sight with 
symptoms of chronic slight optic neuritis, first observed 
about a year before, and still going on. For a long time 
he had been sufficiently anxious to increase the growth of 
hair upon his head as to induce him to use a largely-adver- 
tised preparation, which on analysis was found to contain 
lead. The man brought an action for damages for his 
blindness, and I was consulted. There was no lead line, 
and yet his gums were such as to afford every facility for 
its formation. I felt sure from the absence of the lead line, 
and the fact that the optic neuritis was going on still, 
although it was more than a year since he had discon- 
tinued the use of the preparation, that the condition could 
not be due to this cause. The proprietors of the substance, 
however, afraid of the damage which the mere accusation 
would entail, compromised the matter. This case is an 
illustration of that which may happen to some of you, and 
the importance of the point. Many practitioners have 



236 LEAD PALSY. 

ample opportunities of observing all the effects of lead 
poisoning and of making very important observations ; 
such opportunities may come to some of you, and should 
not be lost. 

A point in treatment to which I have not alluded is the 
use of electricity. That which it can effect is, as in all 
cases of disease of the nerves, to help in maintaining the 
nutrition of the muscles while the nerves are recovering. 
That it can do this to some degree I have no doubt. I 
have seen some clear instances of its service. Before the 
nerves recover, so as to conduct the motor impulses to the 
muscles, the condition of these may be distinctly improved, 
their response to the will promoted, and its degree in- 
creased by the application of voltaic electricity. I remem- 
ber a gentleman who suffered from wrist-drop, and whose 
wife suffered from neuralgia. In neither of them was there 
a trace of lead line, and the cause of the affection had 
therefore been entirely overlooked by at least one very 
eminent physician, the fact that the gums were perfect not 
having been taken into consideration; but the cause was 
suspected by another physician, and it was found that the 
drinking water was charged with lead. From the failure 
to recognise the cause, absolute palsy had gone on in this 
case for nearly a year. There was no power whatever in the 
extensors, and on the first application of electricity not the 
slightest response could be obtained. After several appli- 
cations, however, the muscles began to respond to the 
stimulation, and continued application led to a gradual 
increase in the degree of contraction that was excited, 
until, in the course of a fortnight, they contracted well. 
Soon afterwards slight voluntary power of contraction 
began to return, and it steadily increased, and the patient 
made ultimately a perfectly good recovery. In such a 
case, in wliich electricity so clearly abolished the absolute 
inertia, there can, I think, be hardly any doubt that the 



DUE TO DISEASE OF THE MOTOR NERVES. 237 

local stimulation which voltaic electricity affords to the 
muscles is of definite service, and possibly without it, the 
voluntary impulse would never again have excited them. 

Lead may also cause another form of palsy, not affecting 
specially those muscles, but affecting first the small mus- 
cles of the hand — there is, in this form, gradual wasting 
and gradual weakness, not, as in the extensors, rapid 
weakness followed by wasting. It is a condition identical, 
in its local symptoms, with that of progressive muscular 
atrophy, due to disease of the nerve cells in the cord, and 
probably identical in its seat. It seems to depend on a 
gradual wasting of the cells, fibres, and muscles under the 
influence of lead. In this form, as in progressive muscular 
atrophy, there is merely a diminution of the irritability to 
both forms of electricity, equal, steadily increasing from 
the first, there being no period of lowered or lost faradic 
and preserved voltaic excitability. It may in rare cases be 
wide-spread. Its recognition is of great importance, 
because it does not improve and recover as the wrist- drop 
does. The wrist-drop may pass away entirely and this 
slow wasting away remain unchanged. If the ingestion of 
lead is stopped it does not as a rule increase, but I have 
not known it to pass away. 

Lead palsy in its common form is due to an affection of 
the motor nerves ; the motor nerves to the muscles that 
are affected. The acute atrophic palsy always shows that 
there is an acute affection of the nerve fibres, or of the 
nerve cells from which they spring. Whenever there is 
any acute disease of the nerve fibres, their endings, or of 
their special cells, there is loss of faradic irritability in 
the muscles, and preservation of the voltaic, and there is 
loss of both in the nerves. The electrical reactions do not 
show whether the disease is in the nerves or in the nerve 
cells of the cord ; and until within the last few years it was 
uncertain to which the wrist-drop was due. It has been 



238 LEAD PALSY. 

proved to be due to the nerves, and it has been proved to 
be only one of a series of similar palsies which are due to 
changes in the nerves and are produced by a toxic agent. 
Before we had discerned the characteristics of these re- 
markable toxic palsies, and the evidence that they depend 
on the influence of the poison on the nerves, our uncer- 
tainty regarding its seat was increased by another circum- 
stance, the occasional correspondence in distribution of 
central and peripheral affections. I have already said that 
cases of spinal progressive muscular atrophy sometimes 
begin by rapid weakness of the extensors of the wrist, 
quite like lead palsy, with the same localisation, even to 
the escape of the supinators and of the flexor of the 
metacarpal bone of the thumb. What does this show ? 
It shows that there is a similar pathological susceptibility 
on the part of the motor nerves and on the part of the 
cells from which they come. This is a fact of the most 
profound significance. It shows that the peripheral struc- 
tures and the related central structures suffer in the same 
association. In each corresponding structures have the 
same susceptibility, and seem to have this same associated 
susceptibility to different morbid influences. We can thus 
understand many phenomena otherwise difficult to com- 
prehend. 

Another point regarding the lesion in lead palsy deserves 
attention. Lead palsy is a painless affection, and yet there 
is an acute change in the nerves, a change which consists 
in that rapid alteration of the nerve elements that we call 
parenchymatous inflammation — inflammation of the special 
structure. It is associated with some indications of inflam- 
mation in the sheath and other connective tissue elements 
of the nerve. You know, however, what an intensely pain- 
ful affection neuritis commonly is. Yet here we have a 
neuritis which is painless. What special feature can we 
perceive to explain the difference? The nerve branches 



BILATERAL SYMMETRY DIAGNOSTIC. 239 

affected are those to the muscles; noting that we find other 
illustrations of the same fact. We meet occasionally with 
an isolated one-sided neuritis of a motor nerve ; a motor 
nerve, for instance, of some of the calf muscles, which is 
absolutely painless. The absence of pain, as I have known, 
is most liable to mislead in diagnosis. But remember how 
essentially painless is neuritis of the great motor nerve of 
the head, the facial nerve. There may be pain from asso- 
ciated morbid states, due to the cold that causes the neu- 
ritis, but there is no pain from the inflammation of the 
nerve within the Fallopian canal. It would seem that the 
sheaths of the purely motor nerves and these branches do 
not possess such sensory fibres as most nerve sheaths do, 
and, therefore, their inflammation is not a source of pain. 

Lead palsy, then, is an example of an affection of the 
peripheral nerves from the action of a poison. But it is an 
affection of a few nerve fibres among many of like motor 
function, an affection that is symmetrical, similar on the two 
sides. This is the important fact to be realised by every 
one as the great indication of the whole class of disease to 
which I refer ; the limitation of its functional incidence, and 
with this its bilateral symmetry. These two symptoms in- 
dicate one or two processes, and in many cases they indi- 
cate both. The two processes are degeneration and the 
action of a poison. We are beginning to see in how very 
large a number of instances a process of degeneration is 
the effect of a poison. You will find, if you keep that law 
clearly in mind, that it will guide you right in innumerable 
instances of the most diverse aspect, in which all sorts of 
motor and sensory and reflex symptoms, in various places, 
baffle your efforts to discern their cause, unless you note 
this character and know its meaning-. 

What does the symmetry mean ? Symmetry indicates 
an influence reaching both sides of the body; and if it acts 
on both sides of the body it must be an influence which 



240 LEAD PALSY. 

reaches all parts, because we are unable to conceive an 
influence which acts equally upon certain local parts on the 
two sides and cannot reach others. The bilateral symme- 
try so distinct in the features and the limbs is not a matter 
of the surface, nor is it a matter of the visible form of the 
surface alone. It obtains and must obtain in every struc- 
ture, down to the minute differences of chemical composi- 
tion which underlie function. Parts of the two sides that 
have similar relations and the same functions have, there- 
fore, corresponding constitution, and it is that which is the 
cause of the bilateral symmetry of the effects of any morbid 
influence which reaches both. Consider for a moment 
how belladonna taken by the mouth acts upon both eyes, 
and how perfect that influence may be in limitation and 
symmetry. Consider the minute correspondence of the 
two sides, and the minute difference from other structures 
on each side, which this effect signifies. A similar condi- 
tion alone explains the incidence of lead and other toxic 
agents. You can conceive of no structural relation or rela- 
tion to vessels which determines why lead acts upon the 
branches of the musculo-spiral nerve, and not upon any 
other, and why it acts only on some of the branches. It 
can alone be due to some slight inherent difference in the 
minute constitution of the nerves which enables the atoms of 
lead to join with the atoms and molecules of these nerves, 
and derange the process of their nutrition acting on these 
nerve fibres and not on others. And, moreover, a like con- 
dition is the only conceivable explanation of the fact that 
lead sometimes, and other poisons often, act also on the 
fibres in the legs that are homologous with these fibres in 
the arms, and not on others. When we think of the fact, 
how great is its significance. Those nerve molecules, for 
some reason, have not the power of resistance to a morbid 
chemical agent that other nerves have. They differ in their 
behaviour when a molecule of a metallic poison is pre- 



INFLUENCE OF CHEMICAL AGENTS. 241 

sented to them, although they are the same in the minut- 
est scrutiny we can give them, the same to every other test 
we can apply. Whether any explanation will be found in 
future in some developmental process connected with the 
appearance of these muscles and nerves in the range of the 
animal kingdom, or not, I do not know. But the fact is 
certain that to all these toxic agents these are specially 
susceptible, and the fact is certain that it must be due to a 
greater readiness for the reception of the toxic agent and 
for its influence. 

The various effects of different poisons bring before us, 
in almost startling clearness, how profound is the ultimate 
influence of differences far beyond our power of scrutiny. 
They show us how much of disease that is mysterious may 
be due, in this manner, to chemical agents, and they afford 
us a rational basis for the old faith, not yet lost, perhaps, 
indeed, reviving, in chemical agents as a means of influ- 
encing the processes of disease. 



LECTURE XVIII. 

SATURNINE TABES. 

Gentlemen: — I wish to direct your attention to-day to a 
case that illustrates a subject to which I have repeatedly 
referred during the last few months. I should, indeed, 
hesitate again to refer to it were I not impressed with the 
importance of considering principles and laws, again and 
again, in fresh relations. You will remember that I have 
had much to say regarding the influence of poisons^ — of 
toxic agents — on the nervous system, and that I have 
impressed on you the fact that this is one of the directions 
in which medicine has made the greatest strides during 
the last twelve years. You know in how strange a way 
different poisons act on different parts. Strychnine disturbs 
the function of one part, atropine of another, arsenic of a 
third. You know, also, that this must be an indication of 
some otherwise unrevealed peculiarity in the structures 
acted on. If we observe carefully the effect of the poison 
we see that there is also a considerable difference, which 
depends upon the intensity of the poison. A poison which 
acts suddenly and in large quantity produces effects which 
are much less localised than are those of one that acts 
slowly and gradually. Many parts are susceptible to a 
powerful influence, with much momentum, though only a 
few may be susceptible to the slow influence of smaller 
doses. Intense poisoning by lead may cause wide-spread 

Delivered February 13, 1895. Afedical Magazine, April, 1895. 
242 



VARIED EFFECT OF TOXIC AGENTS. 243 

symptoms, including acute disturbance of the brain ; while 
a gradual, slow poisoning may affect only the extensors of 
the wrists. In diphtheritic palsy we have usually an acute 
toxic process, due to the sudden production of a large 
amount of poison, which acts very widely and very in- 
tensely. But in other cases we may have a slower action 
on some of the limbs. One patient will have universal 
poisoning and muscular atrophy, with signs of nerve 
degeneration. Another patient will have only symptoms 
that present a perfect semblance of locomotor ataxy. The 
important fact that I wish you to realise to-day is that the 
poisons in their slower actions influence the parts most 
susceptible to them. 

Yet to this law we have to recognise some apparent 
exceptions. I especially wish to emphasise the fact of 
exceptions, and the probable cause of their occurrence. A 
poison which usually produces one form of palsy, may in 
another case produce a different form, and yet we may be 
able to perceive no difference either in the amount, or in 
the rapidity with which the poison enters the system. The 
explanation is, I feel sure, that the precise form in which 
the poison is presented to the nerve elements is subject to 
variations. Even the metallic poisons are probably never 
presented to the nerve elements in any simple form. All 
these metallic substances seem to form compounds with 
albuminous bodies, and to be thus presented to the tissues. 
The compound formed depends partly on the dose, partly 
on the form, and very much, probably, on the precise com- 
position and character of the albuminous material, which 
varies in the same individual according to the state of 
health and according to any constitutional peculiarity. 
Hence it is easy to conceive that in a patient with syphilis, 
or in a patient with a gouty constitution, the same metallic 
poison may be presented to the nerve elements in a 
different combination, and may be thus more or less influ- 
ential on function and disturbing to molecular structure. 



244 SATURNINE TABES. 

Why are these compounds so influential ? Because every 
part of the nervous system and of every other system 
(though we are now only concerned with the nervous sys- 
tem) is in a state of constant functional action, and there- 
fore in constant molecular change. Consider how constant 
is the functional activity of the sensory and motor struc- 
tures. We are conscious only of a minute proportion of 
the impressions that are ever traversing even the afferent 
nerves ; while from the motor centres efferent impulses are 
always acting on the muscles, maintaining their tone. This 
fact is true of all parts of the nervous system. Continuous 
activity is the universal law. 

All functional activity is a matter of chemical change. 
The elementary molecules of nerve structure, formed under 
the influence of Life by the processes of nutrition, are dis- 
turbed in their action, and yield some of their constituents 
to the oxygen which is forever lying in wait. They are 
removed, and are instantly replaced, under the same power 
of vital nutrition, from the materials which the adjacent 
plasma has brought to them. And, therefore, if the plasma 
is abnormal in its constitution from the presence of a toxic 
substance, there is constant opportunity for that toxic sub- 
stance to enter into the constitution of the nerve elements. 
However minute the amount may be, no minuteness can 
prevent the results of the persistent appropriation of the 
abnormal molecules. Phosphorus is a normal constituent 
of nerve substance, and you know how close is the relation 
of phosphorus and arsenic. So we can easily understand 
that when arsenic is circulating in the blood it may take 
the place, to some extent, of phosphorus, may enter into 
the nerve elements, may derange function and derange 
nutrition, and, last of all, may derange structure to visible 
degree. 

When the influence of toxic agents acting slowly is con- 
sidered, we find that in all cases it is chiefly on the nerve 
structures furthest removed from the centre on which their 



ACTION ON EXTREMITIES OF FIBRES. 245 

nutrition depends. I explained to you a short time ago 
how we have come to discern that the great function of the 
nerve cells seems to be the nutrition of the nerve fibres. 
The longer the fibre the greater is the distance through 
which that nutritional influence has to be exerted ; and so 
the further the distance from the cell, the feebler this in- 
fluence will be, and the more prone will be the fibre to 
suffer change of nutrition from any cause — the less able 
will it be to resist and reject an abnormal constituent, and 
the more prone to suffer gravely from it. This is probably 
the explanation of the fact, with which you are all familiar, 
that the common effect of these poisons, when they act 
slowly, is to cause degeneration of the peripheral parts of 
the nerves. A few, like strychnine, seem to act on the grey 
matter, but the majority, when in moderate quantity, act 
upon the nerve endings, and in proportion as their influence 
is greater its effect extends further and further up the 
nerve, although it seldom reaches the nerve cell on which 
the vitality of the nerve depends. 

You know the cells in the cortex of the brain, from 
which proceed the pyramidal fibres to the spinal cord. 
These probably end by ramifications related to those of the 
motor cells, whence proceed similar processes which ter- 
minate upon the muscles. From between the muscular 
fibres, and also from the skin, we have afferent nerves 
passing to the ganglia on the posterior roots, and from 
these proceed the fibres that continue the tract, which 
pass — some up the cord and some to the cord at the same 
level. 

As I have just said, if we compare the actions of the 
various poisons, we trace in most a tendency to act on the 
extremities of the fibres, the parts that are most distant 
from the nerve cells. For instance, the pyramidal fibre 
proceeding from the nerve cell in the cortex seems to be 
especially influenced by that peculiar poison which is con- 



246 SATURNINE TABES. 

tained in the seeds of leguminous plants, the effect of which 
is known as " lathyrism," and which causes symptoms of 
lateral sclerosis. Lead acts upon the extremities of the 
motor fibres in certain muscles ; while the peculiar chemical 
poison which we are compelled to assume that syphilitic 
organisms engender seems to act on the parts of the fibres 
of the afferent muscle nerves, and also on the long fibres 
which ascend the cord from the muscles, chiefly in the 
posterior medium column, and seem to subserve cerebellar 
co-ordination. Generally it acts also on the sensory fibres 
from the skin. Alcohol may have the same effects, but 
prefers the motor nerves for the extensors. This is true 
also of arsenic. Both these usually influence the nerves 
of all four limbs, — influence them equally or nearly so, 
both motor and sensory. As I have said, we have curious 
anomalies in these effects. Lead commonly acts only on 
the motor fibres of the arms. You are familiar with the 
fact just mentioned that the poison we assume to be left by 
syphilis — I say " assume," but all analogy makes the 
assumption as near an inference as such reasoning can — 
that it has a special tendency to act upon the muscle affer- 
ent nerves. By this it gives rise to the loss of the knee- 
jerk and to ataxy, of which impairment of these nerves is 
the great cause. Although arsenic and alcohol commonly 
affect motor nerves, each may also affect the afferent nerves, 
including the sensory nerves from the skin, and sometimes, 
for reasons which we do not know, they affect especially 
the afferent nerves from the muscles, and give rise to symp- 
toms like those of common tabes. Indeed, there is more 
than likeness, there is identity — identity of symptoms with 
the slighter cases of true tabes and identity of process as 
far as can be discerned. The alcoholic pseudo-tabes, with 
which you are acquainted, is an affection of the afferent 
nerves from the muscles, probably quite like that of some 
cases of tabes after syphilis. We may have a like condi- 



A CASE PRODUCED BY LEAD. 247 

tion from arsenic. For some reason the poison reaches 
the nervous system in such a form, and the nervous system 
may be so disposed, that the agent acts upon these nerves 
rather than upon any other. Instead of affecting the motor 
nerves, it acts on the sensory fibres, and instead of acting 
on all, it may act chiefly on the fibres from the muscles. 
Lead, however, affects the motor nerves almost exclusively 
— the fact is familiar. Yet there are cases in which it also 
causes loss of sensation. I have recorded a case in which 
lead caused loss of sensation in the skin around the anus, 
apparently from a peculiar action upon the peripheral sen- 
sory nerves. 

Remember this, however, that most agents which act on 
the afferent nerves, influence, in most cases, in greatest de- 
gree those from the muscles. The affection of these nerves 
being the cause of ataxy, we should expect, from all these 
facts, that a form of pseudo-tabes would sometimes be pro- 
duced by lead as it is from alcohol. It has been said to 
occur, but I have never seen an instance, until the patient 
whom I am glad to be able to show you to-day. The 
reason why I have introduced the case to you by this 
roundabout dissertation is in order that you may be able 
to see it without surprise and yet with interest. The action 
which these poisons generally exert, the variations which 
they present in their effect, and in the precise nerves on 
which they act, are such as to make it no matter of sur- 
prise that we should meet with a case in which the afferent 
fibres from the muscles have been chiefly affected by lead. 

You see that the patient walks with his legs wide apart, 
and keeps his eyes fixed on the ground. When he stands 
still and puts his feet together, toes and heels, and shuts 
his eyes, there is far less than normal power of maintaining 
the balance. He cannot, indeed, keep upright. Observe his 
gait more closely as he walks. You see that there is con- 
siderable difficulty in maintaining his equilibrium, but there 



248 SATURNINE TABES. 

is not the peculiar irregular movement of the feet you so 
often see in ordinary locomotor ataxy. The precise symp- 
toms of ataxy depend upon the muscles that are chiefly 
concerned, on what the muscles are, from which the up- 
ward impulses to guide co-ordination are deficient. When 
the muscles whose impulses are deficient, the contraction 
of which has not the proper guiding influence on cord or 
brain, are those of the upper parts of the limbs — those 
connecting the legs and the trunk — there is not the irregu- 
lar movement of the feet which you are accustomed to 
associate with pronounced tabes, not the high step and 
sudden descent of the foot, but there is the unsteadiness 
which you are accustomed to associate with disease of the 
cerebellum. It is a defect rather of the maintenance of 
equilibrium than of the movements of the legs as a whole. 
I now test the knee-jerk. You see that it is absent. 
This is proof that there is an interruption of the path from 
the muscles to the spinal cord — that the common mechan- 
ism of ataxy is here present. The man is a plumber by 
occupation, and there is in his past history one other very 
important fact, namely, that syphilis can be excluded. 
Unless we could have excluded syphilis we should not 
have been justified in attributing this to lead, even though 
we have some of the symptoms of lead poisoning. The 
mere exposure to the risk of the contraction of syphilis is 
found in so many cases to be the only antecedent of un- 
questionable syphilitic symptoms, that we cannot exclude 
syphilis unless we can exclude the common mode of its 
contraction. The hypothetical water-closet is, in my 
experience, purely hypothetical, and need not be taken 
into practical consideration. The only exception to the 
common mode of infection is presented by those who 
attend labours. In this case, then, we can exclude syphilis. 
He has been a plumber since the age of fifteen. There is 
no other cause which we can trace ; although he has never 



DISTINCTIVE SYMPTOMS. 249 

had wrist-drop or lead colic, and yet he has a distinct lead 
line on the gums. These two facts are important. You 
know wrist-drop and colic are common effects of lead poi- 
soning. But here we have evidence of the presence of 
lead in the system in a man who has worked in lead for 
twenty-one years, and yet has not had the common symp- 
toms. From this we may infer that, either owing to per- 
sonal cleanliness or for some other reason, the lead has 
passed into his system in small quantities or in unusual 
combination, and these are the conditions which I have 
indicated as those to which we must look for an explana- 
tion of the occasional anomalous effects of these poisons. 
So that, you see, the very fact that he has been exposed 
to the influence of lead, and yet has never had the common 
consequences, makes it easier for us to believe that this 
uncommon consequence is the result of the lead poisoning. 
He has, moreover, no affection of sensibility, but he has 
had pains not unlike those of ordinary tabes. He has no 
obvious loss of power in his legs, and yet he has a symp- 
tom which at first sight seems to indicate loss of power. 
He has, besides the defective power of maintaining equi- 
librium, a very peculiar difficulty in rising from the floor. 
He can only do so when he helps himself by putting his 
hands on some adjacent object. But he does this, not to 
aid the muscles, but to guide the movement. It is the 
result of the localisation of the inco-ordination to the lower 
trunk muscles, and to the muscles which connect the trunk 
and the legs. In his case it is the symptom which simu- 
lates weakness ; when he is lying, all those muscles are 
able to exert full power. It is of great importance to be 
aware that simple but considerable inco-ordination in those 
muscles may make the assumption of the erect posture 
difficult. When he rises a second time, knowing the reason 
for his difficulty, you will note that, from the very sudden- 
ness by which he manages to get up, there is no defect of 



250 SATURNINE TABES. 

power. He does it now much better than he did when he 
was admitted to the Hospital. A few months ago he could 
not get up by himself, and now, sometimes, he can just 
manage to do so. 

One other point that you should note is this — there is 
no defective action of the pupils such as you so often find 
in true tabes. Although too much weight must not be 
attached to it, the absence of this symptom is always some 
reason for thinking that tabetic symptoms are due to some 
other poison than that which usually causes them. 

He has not much lead line, and I should like you to 
notice that it is only to be seen where the gums are de- 
tached from the teeth. I have before explained to some of 
you the way in which the lead line is produced. When 
the gum is in perfect apposition to the teeth there is no 
leadline. The lead line is sulphide of lead deposited just 
beneath the surface, outside the tiny loops of vessels — a 
disposition which gives it a granular aspect under a lens. 
A layer of such sulphide of lead is deposited beneath the 
inner surface of the detached gum, and it is the edge of this 
layer that is seen as a line. The sulphur comes from de- 
composing albuminous materials lying between the tooth 
and the detached gum. Unless albuminous materials lodge 
there, no sulphide of lead is formed, and there is no lead 
line. I have seen cases of extreme lead poisoning, with 
perfect gums, and with no trace of lead line. But yet, as 
most people have somewhere a space between the edge of 
the gum and the teeth, sulphur-yielding materials accumu- 
late there and form at least a fragment of lead line. It is 
instructive here to notice that the line is confined to those 
two teeth in which the gum is detached, and that against 
the others, to which the gum is in close apposition, there 
is no line. 

The treatment of such a case is, first, the ordinary treat- 
ment for lead poisoning ; and, secondly, when the toxic 



TREATMENT. 251 

influence has been entirely removed, we should attempt to 
help the processes of regeneration by agents, such as 
strychnine, which seem to promote the nutrition of the 
nerve elements. I will, however, only add this injunction : 
Remember that all these metallic poisons become stored 
up in the tissues as compounds with organic substances, 
and the first effect of releasing them from the tissues is to 
increase the quantity in the blood. Give iodide of potas- 
sium in lead poisoning and the amount of lead is increased 
in the urine. Iodide of lead is insoluble, but the lead forms 
a soluble combination with the iodide and albuminous 
bodies which can pass from the tissues into the blood and 
away by the excretory organs. At first the quantity of 
lead in the blood may be very much increased, and its re- 
sulting effects also increased. Some of you will remember 
a remarkable case of arsenical poisoning with nervous 
symptoms and rash, which I showed last summer. Iodide 
has a like effect in arsenical poisoning. In that patient the 
iodide had to be discontinued, so greatly were the symp- 
toms aggravated by the irritation of the arsenic which the 
iodide brought from the tissues into the blood. These 
symptoms continued for a long time, but now the patient is 
practically well, except for some pigmentation which still 
persists. The recovery from these effects is slow; happily, 
however, it is, as a rule, sure. As the lead passes from the 
nerve elements their vital power of nutritional renewal en- 
tails a slow restoration of structure and of function, and 
although, in this patient at present, improvement is slow, it 
is definite, and we may anticipate that it will progress to 
restoration of the normal state. 



LECTURE XIX. 

OPTIC NEURITIS. 

I. — Slight. 

Gentlemen : — My task to-day is to endeavour to help you 
to help yourselves. There are some things that may be 
taught by another, but there are many things which the 
learner can only teach himself, and it is with one of these 
that I want to occupy your attention to-day. I will do so 
for less than the usual space of time in order that you may 
have time to learn by observation that which you can only 
learn in this manner. And I do so because I happen to 
have the opportunity of affording you the means of observ- 
ing a case which is almost unique in its characteristics and 
in the instructive points that it presents. There is one 
symptom only to which you need attend. The other 
symptoms are so uncertain in their significance that it is 
doubtful whether it is worth while for me even to bring 
them before you for their negative significance. 

The symptom which is presented is optic neuritis. The 
unusual features which it presents are that it is neuritis in 
one eye only, and that in this eye the neuritis is partial. 
Any of you can come at another time and examine the 
patient carefully at your leisure. 

You probably know that it is rare for optic neuritis to 
be one-sided. It is one of the symptoms which usually 
occur on both sides at the same time, because, as a rule, 
its cause is either an influence from the brain, which acts 

Delivered October 24, 1894. Clinical Journal, December 5, 1894. 

252 



ABNORMAL DEVELOPMENT. 253 

equally upon the two sides, or an influence from the blood, 
which likewise has an influence so general that its effects 
are bilateral. Whenever you can compare one side that 
is normal with the other that is diseased, whatever kind of 
disease it may be, you are always at much greater advan- 
tage in your observation than when there is perfect bilateral 
symmetry in the morbid change. Many slight morbid 
changes are difficult to recognise in their absolute degree, 
and yet not difficult to recognise if there is the opportunity 
for comparing an absolutely normal state on one side with 
the slight abnormal condition on the other. 

The case is instructive not only on account of these 
features, but because the neuritis has developed in a pre- 
existing condition that is itself abnormal — a condition which 
depends upon an extreme degree of myopia. This fact 
adds to its practical utility to advanced students, because a 
considerable degree of myopia increases the difficulty 
of observation and the risk of error ; and thus the 
careful study of the case will not only give you definite 
information, but will also increase your ability to overcome 
a difficulty which is not uncommonly met with in ophthal- 
moscopic work, observation under the condition of con- 
siderable myopia. As you probably know, this difficulty 
only obtains in the direct method of examination, in which 
there must be accurate compensation by a lens behind the 
ophthalmoscope. I fear I seem to be making the advan- 
tages of the case depend on its difficulties, but, in point of 
fact, every great difficulty that is overcome lessens a host 
of minor difficulties. I may further press on you the 
necessity for careful estimation of the conditions under 
which you are observing, inasmuch as the myopia here is 
almost twice as great on one side as on the other. If you 
try to compensate on one side in the same degree in which 
you compensate on the other, you will be unsuccessful. I 
therefore impress upon you the necessity, in the first place, 



254 OPTIC NEURITIS. 

of always observing and ascertaining what are the condi- 
tions under which you are making your observation. 

This necessity is very important in all diseases. Students, 
and I fear sometimes those who are no longer nominal 
students, listen to the apex of the heart where the apex of 
the heart ought to be, instead of at first ascertaining where 
it is. I have frequently known a student fail to find a 
murmur at the apex of the heart, because he was listening 
where the apex ought to have been, not where it was. The 
patient who is before you has a cardiac condition worthy 
of observation, although it will not involve that difficulty. 
There is a loud murmur at the apex, but it extends so 
widely that you will not miss it, even though you miss the 
apex and have not done what you always should do — feel 
where the apex is before you listen. It is a systolic mur- 
mur, and there is also a systolic murmur at the base, which 
is certainly a separate murmur. Never omit carefully to 
observe collateral symptoms. You will examine this case 
on account of the condition of the eyes, but it can teach 
you a good lesson in auscultation of the heart ; and if you 
have another opportunity of examining the patient you 
should make a careful examination of the heart. When 
there is a systolic murmur at the apex and a systolic mur- 
mur at the base, the one due to aortic stenosis and the 
other to mitral regurgitation, it is generally not difficult to 
ascertain the fact that there are two murmurs if you are 
sufficiently careful to observe the gradation of the sound, or, 
rather, the sequence of reversed gradation, in passing from 
the apex to the base. The pure mitral murmur becomes 
fainter ; if it does not, and is even louder at the base and 
over the aortic orifice than at the apex, you may feel sure 
that there is aortic constriction, and especially if, as in this 
case, you can observe a change in the quality of the mur- 
mur. I mention this because the co-existence of mitral 
regurgitation and aortic stenosis, without aortic regurgita- 



METHOD OF EXAMINATION. 255 

tion, is not very frequent, and whenever it is met with it 
should be most carefully observed, because it is not always, 
for the reasons I have mentioned, easy to detect. 

I said that the difficulty involved in myopia is chiefly in 
the direct method of examination, but a fallacy is caused 
by myopia in the indirect examination. In this method, 
the optic disc looks small in myopia and large in hyper- 
metropia. Just as you should always, before listening to 
the apex of the heart, find out where the apex is, so, before 
looking into the eye, you should ascertain roughly what is 
the state of refraction. That is easy to do. First throw 
the light into the eye by the mirror from a distance, from 
the distance you would adopt in the indirect method of 
examination. Move your head a little, and you will 
quickly catch sight of a vessel. If you see that vessel 
distinctly, the refraction is not normal ; there is either 
myopia or hypermetropia. Move your head again a little 
to one side or the other; if the vessel seems to move in the 
same direction, there is hypermetropia; if it moves in the 
opposite direction, there is myopia. You then know what 
to do when you proceed to the direct method of examina- 
tion, and you know how to estimate the size of the optic 
disc as it appears to the indirect method of examination. 

This case illustrates the fact in a curious way. I show 
you large, somewhat rough drawings of the discs, and I 
have here also a more careful drawing which you can com- 
pare with what you see when you examine the patient 
(figure). In the left eye (on the right, in the figure) the 
optic disc, of oval outline, appears larger than you would 
expect. It looks larger than the normal disc, although the 
eye is myopic, and in myopia objects should look small. 
It is not the optic disc you see. Note that there are two 
oval outlines ; the optic disc is the inner area, and the outer 
boundary is simply the limit of what is called a " posterior 
staphyloma;" that is, an area of atrophied choroid, so 



256 OPTIC NEURITIS. 

common in myopic eyes in consequence of the greater 
length of the eyeball. The tendency to increase in length 
leads to a condition in which the opening in the choroid 
does not reach the opening in the sclerotic, and is increased 
by a process of atrophy of the choroid. 

This case has still further the utility that the arrange- 
ment of the vessels is particularly puzzling, and if, with the 
help of the drawing, you discern them perfectly, you will 
have enabled yourselves to overcome many other difficul- 
ties which you will meet with afterwards in other cases of 
peculiar vascular arrangement. The peculiarity here is 
that the central artery is so situated as to entirely conceal 
the origin of the veins. In the left, the normal disc, you 
see in the middle the white area of the physiological cup, 
and the vascular portion of the disc extends up to the 
place at which the vessels emerge. If you are familiar 
with normal eyes you will know that that is very frequently 
the case, especially when the physiological cup is large. 
The dark portion on the other side of the cup is greyish in 
tint and not vascular. I have purposely had these dia- 
grams done in black and white and not in colours, for the 
same reason that I had most of the drawings in my 
" Medical Ophthalmoscopy" done in monochrome, be- 
cause it is of considerable more importance to attend to 
the changes of form than to the change in colour. Nine- 
tenths of that which is important in the disc depends on 
change in form — on that which can be shown in black and 
white, and not in change in colour — and nine-tenths of the 
errors that are made in interpreting the appearances are 
owing to undue weight being given to changes in colour. 
I should hardly like to say how many cases of normal 
discs I have had shown to me, as the seat of optic neuritis, 
simply because the discs were highly coloured. The vas- 
cularity of the disc varies as much as does that of the 
cheek. The test of a morbid condition is not the colour, 



ILLUSTRATIVE DIAGRAM. 257 

it is the change in form, — it is especially obscuration of the 
edge. 

In this optic disc, the arteries, as I say, happen to be so 
placed that they entirely obscure the portion of the veins 
where the branches unite to pass into the nerve, and it is 
only on very careful observation that you can discern which 




Partial optic neuritis in the right eye only. Both eyes are myopic. In 
the right (the patient's left) there is a posterior staphyloma extending all 
round the disc. The cup is steep on the nasal side (to the right in the 
drawing), which is of the inverted image, so that in this disc the side fur- 
ther from the other eye is really the nasal, and the darker tint on the 
sloping side of the cup (apparently towards the other eye, but the tem- 
poral) is due to pigment. The emerging mass of nerve fibres extends up 
to the vessels on the other side. 

In the left eye a similar condition is seen in rather less than half the disc ; 
that apparently towards the other eye and therefore really away from it, 
i. e., the temporal side. The side further from the other eye, that is, the 
real nasal side, is obscured by inflammatory swelling, which presents also 
some small hemorrhages. The clear side, really the temporal, is of course 
the side turned towards the yellow spot, in which the nerve fibres are few 
or absent. The figure shows the tendency of neuritis to develop first 
where the nerve fibres pass off and the interstitial tissue is abundant. 



are arteries and which are veins. The veins seem to arise 
from the arteries. It is always necessary to look carefully, 
to be quite sure, especially in the case of smaller vessels, 
which is an artery and which is a vein. It is the colour 
and the character of the central reflection that distinguish 
them. 



258 OPTIC NEURITIS. 

Turning to the other eye, we see a condition which is 
also most instructive. Here also the venous branch is 
obscured at the beginning by an artery. The upper vein 
is the most conspicuous object that attracts attention. On 
looking at the disc, you will be struck by the fact that at 
one side there is a pale, or almost white zone, pretty sharply 
margined on the outside, and limited inside by a redder 
zone. The outer white zone is a condition of choroidal 
atrophy, revealing the sclerotic, — a "posterior staphyloma," 
similar to that which is seen in the other eye. The disc 
itself begins at the inner oval. As the figure shows, the 
edge of the disc is distinct on one side, but is entirely lost 
upon the other. There, you can see no margin to the disc, 
and you can see no zone in which the white sclerotic is 
visible in consequence of atrophy of the choroid. It is all 
covered by a faintly striated, red tissue. On the inner part 
of this there are several small but distinct hemorrhages. 
The amount of swelling is slight. Swelling can be esti- 
mated accurately by ascertaining what strength of convex 
lens behind the ophthalmoscope is required to make indis- 
tinct the surface of the swelling compared with the adjacent 
retina, or, in the case of myopia, what difference in the 
strength of concave lens is required behind for distinct 
vision of each. That is, however, a difficulty in myopic 
eyes, and you can generally, without much difficulty, esti- 
mate the amount of swelling in two other ways. First, 
whenever there is much swelling, the central reflection of a 
vein is lost where it descends the side of the swelling. You 
know the cause of the central reflexion from the middle of 
a vein. That which we call a retinal vein is not the vessel, 
but the column of blood within it ; and from the centre of 
the convex column of blood the light is reflected straight 
back to the eye, whereas from the lateral parts the light is 
reflected at an angle. The consequence is that all the light 
is reflected from the central part of the convexity, and this 



ESTIMATION OF THE SWELLING. 259 

prevents the colour of the blood being perceived as at the 
sides. 

But supposing a vein slopes for a short distance, so that 
its course is in a plane at an angle with the direction of the 
light other than a right angle. The central reflection is 
only seen where the vein is running in a plane perpendicu- 
lar to the line of sight. In a part at which the vein slopes, 
there is no central reflection, and so the vein appears darker, 
because in the centre the colour of the blood is seen as it 
is at the sides. Therefore, whenever there is the appear- 
ance of swelling of the disc, observe most carefully the 
veins as they pass on the sides of the affected area, and 
notice whether there is loss of the central reflection. If 
there is considerable swelling there is sure to be this loss. 
In this case it is scarcely perceptible, and therefore the 
amount of swelling is slight. The other method bv which 
the amount of swelling can be easily estimated ought to be 
familiar to you, because it is of such wide application to 
every condition in which there is a difference in the level 
of objects in the fundus; as, for instance, to the depth and 
shape of the "cup." It is that which is called "parallactic," 
because, by an almost presumptuous use of a word which 
has a wide and important meaning to designate an exceed- 
ingly small subject, the word which describes the means of 
ascertaining the millions of miles of distance of the earth 
from other planets is applied to ascertain whether one object 
in the fundus of the eye is a millimetre in front of another. 
It depends simply upon the fact that the relative position 
of two objects is different if you change your point of view. 
In the case of the ophthalmoscope, — if, in the direct method, 
you move your head a little to one side and back again; 
if in the indirect method, you move your lens in the same 
way, — you see a change in the relative position of the 
objects. In astronomy it is necessary to wait until the 
other side of the earth's orbit is reached to observe the 



260 OPTIC NEURITIS. 

change in the relative position, but the principle is essen- 
tially the same. Never omit an opportunity of practising 
it in ophthalmoscopic work. Whenever you look at even 
a normal disc, move the lens a little, or move your head in 
the direct method, and you will be surprised how the rela- 
tive change of position of objects at the edge of the disc 
and at the bottom demonstrates to you their relative dis- 
tance almost as perfectly as if you were looking through a 
stereoscope. 

The great fact of optic neuritis is the blurring of the 
edge of the disc in consequence of increase of tissue in 
front of it. The opacity of the tissue prevents the normal 
reflection of that which is behind, which can pass without 
difficulty through the quite translucent normal structure. 
Remember that the blurring always begins upon one side. 
You know that the nerve fibres which come from the optic 
disc, and radiate on the retina, come off on the nasal side, 
and above and below, but scarcely or not at all on the 
temporal side, towards the yellow spot, in spite of the fact 
that the yellow spot is the centre of vision. Hence it is 
that, at that part of the disc, the structures are absent, the 
nerve fibres, and the tissue between them that is the chief 
seat of inflammation, present the first visible signs of 
neuritis. When it is intense and considerable, there is 
sufficient tissue, even where it is least, to permit inflamma- 
tion to invade the whole periphery of the papilla ; but 
when it is slight the changes are limited to the side on 
which they are first seen. This is well seen in the figure 
before you and in the patient from whom it has been 
drawn. I am anxious that you should carefully observe 
it. The inflammatory change obscures the edge above and 
below, and on the whole nasal side, while it is absent on the 
temporal side. 

In normal states there is always such transparency of 
the structures in front of the edge of the disc as to enable 



OPHTHALMOSCOPIC EXAMINATION. 261 

you to see it, even where the nerve fibres are most abun- 
dant. The first effect of neuritis is to increase the ob- 
scuration by making the tissue which is over the edge 
less translucent, and so to cause the apparent " blurring." 
Thus indistinctness of the edge is the first manifestation 
of the process. But the edge may be indistinct from 
another condition. You may have much difficulty in see- 
ing it because the outer part of the disc is so red as to be 
of the same tint as the choroid. It is through this that the 
mistake is often made to which I have referred, the mistake 
of thinking that a disc that is simply and naturally red, is 
inflamed. This important distinction, however, is not diffi- 
cult. The rule that you should fix in your minds is this. 
Let me first explain its reason. When you look with the 
indirect method, the degree of magnification is low, the 
illumination wide, and focus deep ; when you look with 
the direct method, there is a much higher degree of mag- 
nification, and a much more limited illumination and shal- 
lower focus. It is so with the microscope ; a low power 
affords a considerable depth of focus ; with a high power 
you have a very shallow range of focus. Hence, when you 
use the ophthalmoscope by the direct method, with its high 
magnification, you have a very shallow layer of focus 
compared with that which is afforded by the lower power 
of the indirect method. Hence it follows that if there is 
anything in front of the edge of the disc, obscuring it, 
when you examine by the direct method this layer is 
focussed, and not that which is behind it ; the latter is not 
perceived, partly as it is not in focus, partly as that which 
is before it is in focus and so is distinct. With the indirect 
method, however, a lower magnification, a deeper focus, 
and a greater illumination enable us to see distinctly the 
tissue in front of the edge of the disc and also that which 
is behind this tissue, the edge of the disc itself. With the 
direct method, real obscuration is greater than it is with the 



262 OPTIC NEURITIS. 

indirect. But if the edge is indistinct from resemblance 
in tint of the disc to the adjacent choroid, when the eye is 
examined with the direct method the edge of the disc is more 
distinctly seen. Thus there follows this most important 
rule, that, if you think there is commencing neuritis, when 
the appearances are more natural with the direct method 
than with the indirect, it is normal ; they are more morbid 
when there is more obscuration with the direct method. 
This is a rule of great practical importance; you may 
trust it, and if you endeavour to apply it you will soon dis- 
cover its value. 

I intended to describe to you the symptoms which the 
patient presents, but I think it is not worth while to do so, 
because the case is one in which a precise diagnosis is im- 
possible, and in which the process of attempting to make a 
diagnosis is not of such conspicuous use as to justify me 
in diverting your thoughts and over-crowding to-day's 
memory. She has slight weakness on one side, a history 
of some giddiness, and of some headache of varying degree. 
A little weakness is thought to exist in the external recti, 
but it is not conspicuous. There is no nystagmus, and if 
it were not for the optic neuritis I think we should scarcely 
be inclined to consider that there was any organic disease. 
It is one of those cases in which there may be a small 
slowly growing tumour in some situation, or a tumour 
which is stationary, or increasing only at intervals as a 
tubercular tumour may do. But the symptoms themselves 
do not indicate tumour, nor does the optic neuritis. 

The last statement may surprise you. The chief and 
first significance of optic neuritis is the presence of organic 
disease. If you can exclude a blood-state, or constitutional 
condition, you may feel sure that there is organic change 
within the skull or orbit, such a change as could be recog- 
nised almost always with the naked eye, and always at any 
rate with the microscope. The organic brain disease caus- 



ITS DIAGNOSTIC SIGNIFICANCE. 263 

ing neuritis is of an irritative character. Irritation is the 
one element with which we can connect the process of 
neuritis, but the questions of mechanism and causation I 
must deal with upon another occasion. The point I wish 
now especially to press upon you is that, when neuritis is 
due to intracranial organic disease there is a relation be- 
tween the course of the morbid process in the brain and 
the visible inflammation within the eye. Hence, neuritis is 
important, not only for diagnosis, but for prognosis. Many 
times I have known the commencing subsidence of neuritis 
to be the first indication of the commencing subsidence of 
a morbid process in the brain, and I have known the per- 
sistence of neuritis to be the indication of persistence of 
disease in the brain, of which every other effect, for the 
time being, had passed away. In each instance, and each 
class of instances, the indications have been absolutely 
verified. Further, chronicity indicates chronicity : chron- 
icity of the neuritis, chronicity of the process. The con- 
verse is not always true. A chronic process in the brain, 
going on slowly, sometimes causes an acute development 
of neuritis. Doubtless the exception is only apparent; 
some acute consequence of a chronic growth causes the 
acute neuritis. A rapidly growing tumour never causes a 
chronic neuritis. 

Neuritis is, however, sometimes so chronic that you may 
watch for month after month, and observe no change, and 
then, if there is organic disease, you can be certain that it 
is of a most chronic character. That is the case with this 
patient. I say, " If you can be sure of organic disease," 
because I have seen cases of slight optic neuritis of extreme 
chronicity in which, although there was no constitutional 
condition to explain it, I could not be sure of organic dis- 
ease. Indeed, I have sometimes felt sure there was no 
organic disease. Those cases at present are a mystery. In 
a few cases, during a year or two years, I could see no 



264 OPTIC NEURITIS. 

change in the aspect of the discs, and in one of them I 
came to the conclusion that it was a congenital condition. 
But conclusions, gentlemen, seldom merit their name. 
Most conclusions should be regarded as beginnings, and 
not as endings, if you can pardon the paradox ; it happened 
that five years afterwards I saw this patient, and every 
morbid appearance had passed away. It is possible that 
hypermetropia aids in the development of the condition. 
But all the patients, to whom I refer, presented evidence of 
functional disturbance of the brain, and I think there are 
cases in which very chronic optic neuritis is due to the 
combined influence of what we call " functional " brain 
affection and hypermetropia. How these causes act is still 
a very open question. But in none of those cases was the 
process sufficiently active to lead to extravasation of blood, 
and although in this patient, during the four months she 
has been under observation, no change has been percepti- 
ble in the optic neuritis, there have occurred the small ex- 
travasations of blood, which show an activity that is defin- 
ite and seems to take the case out of the category of those 
that I have just been referring to. (Here again I have to 
guard the statement.) I say " seems," because the features 
suggest the question whether the occurrence of the extra- 
vasations may not be specially related to the peculiar 
arrangement of the tissues and vessels, and therefore 
whether it has so much meaning as we can generally 
ascribe to them. Remember that exceptional facts are 
often related, and that an unusual condition may be the 
cause of an unusual feature — that the preceding, congenital 
state here may be the reason why there are such hemor- 
rhages as are scarcely ever observed in neuritis that is at 
once so slight in degree and so extremely chronic in its 
course. 

It will be more useful for you to carry away, instead of 
a confused perception of the possible meaning of the other 



EXCEPTIONAL CASES. 265 

symptoms presented by the patient, a clear perception of 
this one fact. There are cases of optic neuritis in which 
the process has not its common significance. There are 
cases in which it does not even help us to say that organic 
disease is present, in which it leaves the diagnostic problem 
very much as it would be without the neuritis. It should, 
indeed, invariably have one effect upon our minds. Like 
many other symptoms, in many other morbid states of 
various kind and in every part, it should make us more 
watchful, more careful to maintain our observation, and 
more ready to give due weight to any unequivocal symp- 
tom that occurs, — remembering ever that symptoms that 
are unequivocal alone may be decisive when combined. 



23 



LECTURE XX. 

OPTIC NEURITIS. 

II. — Severe. 

Gentlemen : — A few weeks ago I drew your attention to 
a case of optic neuritis of peculiar instructiveness on account 
of its slight degree and unilateral character. One eye was 
normal, the other presented the least degree of definite 
neuritis on one half of the disc. Although the nature of 
its cause was uncertain, we could not doubt that the changes 
were due to an intracranial process. I may add that the 
condition has since undergone little change, sufficient to 
show no more than the fact that it is not stationary. 

To-day I wish to take an opportunity, although it is an 
imperfect opportunity, of presenting to you the features of 
a case of optic neuritis which stands at the other end of the 
scale. This, also, is due, without doubt, to intra-cranial 
disease ; but instead of being slight in degree, it is one of 
the most severe I have ever seen ; indeed, it is, on the whole, 
the most severe I have seen. I am, therefore, unwilling 
to lose the opportunity of impressing on you the features 
of this important symptom in its extreme degree. Although 
the patient is before you, I am sorry that I cannot invite 
you to examine her as you examined the other patient. 
It may be practicable for you to come at some other time 
and look at her eyes, but she is enduring such severe 
paroxysms of pain that even movement down into this 
theatre is as much as it is right to subject her to. But I 

Delivered January 16, 1895. Clinical Journal, June 5, 1895. 
266 



INTRA-CRANIAL GROWTH DIAGNOSED. 267 

will tell you the salient facts of the case, and the mere 
sight of the patient will impress them upon you. 

She is a young woman, aged twenty-two, who has lost a 
brother from consumption. Last June, seven months ago, 
she began to suffer from headache. It was at first slight, 
but quickly became severe ; partly frontal, and partly occi- 
pital. Transient weakness of the left internal rectus was 
observed. The headache and the diplopia led to an oph- 
thalmoscopic examination, and the observer, a country 
practitioner, found, to his surprise, intense optic neuritis ; 
so intense and considerable that it must have either devel- 
oped with extreme rapidity or must have existed for some 
time before the headache began. The neuritis suggested 
a tumour, and she was treated with large doses of iodide of 
potassium. The common procedure, whenever there is 
reason to suspect an intra-cranial growth, is the adminis- 
tration of iodide of potassium, because a growth is some- 
times due to syphilis. This treatment is adopted rightly 
when this cause is possible, but occasionally without ade- 
quate perception of the fact that it is impossible, although 
this fact, sometimes, be clearly discerned. The treatment 
increased her discomfort. I cannot say that it did her 
definite harm, yet you should know that this treatment may 
have, indirectly, disastrous results. The most intense optic 
neuritis, precisely like that of cerebral tumour, may be due 
to anaemia, at any rate to the chlorotic anaemia of girls. I 
have seen a case of such neuritis which was only discov- 
ered when sight had become gravely impaired, and then, 
although syphilis could be absolutely excluded, the case 
was treated with iodide of potassium until all sight had 
vanished. In the case referred to, I am certain that the 
prompt administration of iron, combined with perfect rest, 
would have secured the recovery of a fair degree of sight 
if not of perfect vision. I have known cases in which, I 
am sure, sight has thus been saved. I mention rest, be- 



268 OPTIC NEURITIS. 

cause, in what may be called a critical state of anaemia, it 
is of the utmost importance that the deficient haemoglobin 
should be saved for vital processes. In these cases, so 
different from pernicious anaemia, the defect is in the haemo- 
globin, in the element that carries oxygen to the tissues. 
The first thing is to prevent the inadequate supply of oxy- 
gen being wasted in the release of energy from the muscles. 
Without adequate oxygen the machinery of life cannot be 
maintained in the needed power. The first essential is to 
save for this the oxygen it would waste in energy. That 
patient has now been for several years, and will be, as long 
as she lives, absolutely blind. 

Thus, you will perceive, that, while the administration of 
iodide of potassium cannot have, in such cases, much bene- 
ficial influence, and, probably, has none, it is not unim- 
portant because it hinders the adoption of proper treatment. 
It is doing something, but this therapeutic refuge does not 
always illustrate the maxim that" something is better than 
nothing." It may be no worse than nothing, yet there 
may be another comparison — there maybe something else 
which might be done, and which would save that which, to 
many, is more precious than life itself. If it is, in general, 
true that " knowledge comes and wisdom lingers," we must, 
alas, admit that knowledge is too slow of foot and is too 
long in spreading. That which is not often needed, 
not often enforced by observation, however simple it may 
be, however practical, seems to find no holding-place, and 
when urgent need arrives, it is not there. 

But this is " by the way." We must leave it and come 
back to our patient's history. Her medical history is 
somewhat of a blank for a time, save for the fact that her 
sight slowly failed. A month or six weeks ago she could 
just count fingers with one eye, but since then she has lost 
all perception of light. 

She now comes here with headache, paroxysmal, but 



INTRA-OPTIC CHANGES. 269 

most intense. Up to about three weeks ago the headache 
had been but slight, but during the last three weeks it has 
become much more intense, although still paroxysmal, and 
it has been more prominently occipital, and more on the 
left side than on the right. During the paroxysms there 
has been a little retraction of the head. Once or twice 
vomiting has been associated with it, but vomiting has not 
been a conspicuous symptom. She is able to stand, but 
shows a little unsteadiness. There is a history of occa- 
sional slight attacks of subjective sensation of" numbness " 
in the left arm. There is no foot-clonus ; the knee-jerk is 
excessive. There is not now any distinct difficulty in the 
movement of the eyes, or paralysis of any cranial nerves. 

With such a headache, combined with optic neuritis, it 
is impossible to doubt that she is the subject of an intra- 
cranial growth. These indications are the more definite 
because the headache is occipital. Optic neuritis in anaemic 
girls may be associated with very severe headache, but this 
is general or is greatest in the front of the head. It is also 
more or less constant — not paroxysmal, as in our patient. 
Moreover, what is of great practical importance, there is no 
sign of definite anaemia, which, were this optic neuritis of 
anaemic origin, would unquestionably be conspicuous. 

You can see, even from a distance, the blind look of her 
eyes. You can see the large pupils which, I may say, do 
not act to light, and you can also see the slight retraction 
of the head. If, as we know, there is optic neuritis of great 
degree, the absence of reaction of the pupils becomes un- 
important. But if a patient has optic neuritis in very slight 
degree, insufficient to impair sight, the absence of any 
pupillary action would show conclusively more consider- 
able morbid process in the optic nerves, or at the chiasma. 
Here the changes within the eye are ample to account for 
the loss of sight and of action of the pupil. 

It is to these changes that I desire to draw your atten- 



2-jo OPTIC NEURITIS. 

tion. Although you cannot to-day observe them for your- 
selves, I am fortunate in being able to put before you two 
admirable drawings of the fundus, by Dr. Ridley (repro- 
duced in the accompanying figures). In the left eye you see 
a pale area, not much bigger than the disc, soft-edged, and 
distinctly prominent, as the curves of the vessels show, and 
as is also shown by the change in their central reflection. 
But there are also changes in the retina, white spots and 
flakes and streaks, not only around the macula lutea, but 
on the opposite side of the optic disc. Beyond the side of 
the papilla, which is away from the yellow spot, there is a 
conspicuous series of such flakes, unusual as a consequence 
of neuritis. Note also that between that and the disc there 
is a curved line, lighter than adjacent fundus, concentric 
with the disc. Such a line is seen occasionally in cases in 
which the optic neuritis has been very much more exten- 
sive than at the time when it was observed. It is due to 
the swelling of the substance of the papilla, which, pushing 
away the adjacent retina, has thrown it into a fold. You 
will find illustrations of the process in " Medical Ophthal- 
moscopy." I have seen two, or even three, such folds 
under the microscope. During the height of the inflamma- 
tion they are inconspicuous, but they remain when the 
process has subsided. We shall presently have to note 
their earlier stage. In consequence of the reflection of light 
from the convexity such folds appear as pale lines. 

This condition indicates a neuritis which has to a con- 
siderable extent subsided. At a previous period the papilla 
no doubt presented very much the aspect which the other 
papilla now does. Although neuritis is usually double, it 
frequently develops somewhat earlier in one eye, and often 
reaches its greatest intensity in one eye sooner than in the 
other. So it is in this patient. The one eye is in the stage of 
subsidence, while in the other the process is at its height. 
To this, as shown in the other figure, we will now turn. 



PRIMARY PAPILLITIS. 



271 




272 OPTIC NEURITIS. 

The appearance in the right eye in which the condition 
is in the acute stage is such as I have never seen before 
from intra-cranial disease. Indeed, I have never seen the 
like from any cause ; I have never seen such extensive 
damage to the retina in any other case of primary papil- 
litis, such as this undoubtedly is. In the position of the 
papilla is a wide prominence four times * the width of the 
normal optic disc. (The photographic reproduction has 
rendered the swelling too dark.) You will notice that its 
soft edge is broken by radiations, at which the whitish tis- 
sue extends further on the retina. It amounts in the left 
eye to four diopters, and probably to six in the right. But 
the most remarkable feature is the extent of damage to the 
adjacent retina. I called your attention in the left eye to 
the white dots and flakes about the macula and on the 
other side of the papilla. The same are seen in the right 
eye, but in this they are arranged all around the macula 
lutea in a double range, and also around most of the 
circumference of the disc. On the side opposite to the 
macula they extended beyond the area that could be 
brought into the figure. f 

In " Medical Ophthalmoscopy " you will find a figure of 
a case of intense optic neuritis which had involved the 
retina to as wide an extent in the active process, as it is 
here involved in the inflammatory swelling, but the draw- 
ing was made after the subsidence of the inflammation. 
Around the macula, white spots and flakes were left, very 
nearly the same as those shown in the drawing of the right 

* The gradation of the edge of the right neuritic swelling is too sharp and 
the swelling is too white in the figure, which is, indeed, a very inadequate re- 
production of the excellent drawing of Dr. Ridley. The actual diameter of 
the disc would not be more than three-quarters of that of the pale area. 

f An important paper on the relation of these flakes to the structure of the 
retina and to oedema, by my colleague, Mr. Marcus Gunn, will be found in the 
" Transactions of the Eighth Ophthalmological Congress," 1884, p. 77. 



RENAL COMPLICATIONS. 273 

eye of this patient. The figure in " Medical Ophthalmos- 
copy " is from a case of optic neuritis due to anaemia, not 
to an intra-cranial cause ; it was primarily an inflammation 
of the papilla and not of the retina, but involving the retina 
secondarily. 

The fact that these changes in the retina resemble those 
of albuminuric retinitis is one of very great practical im- 
portance. A case such as this, in which each eye presents a 
subsiding neuritis, with changes about the macula lutea of 
this character, may accompany symptoms of intra-cranial 
tumour which are not decisive, and there may be also some 
albumen in the urine. You can imagine how difficult it 
would be in such a case to decide whether the changes 
were due to kidney disease or were the result of previous 
intense neuritis from an intra-cranial cause. The difficulty 
is not hypothetical. I have met with the combination and 
with this difficulty, especially in young women and in 
children. The albuminuria has been slight ; there has been 
no evidence in the urine or elsewhere, of structural kidney 
disease, and there have been symptoms of intra-cranial 
tumour, suggestive though not conclusive. But in the cases 
in which the retinal changes are secondary the papilla 
always presents the features which indicate a considerable 
previous inflammation. Knowing that such neuritis will 
lead to these changes you should have no difficulty. It is 
only when the neuritis is slight, and there is no great 
amount of new tissue in the papilla that albuminuric retinitis 
should be thought of. 

But there is another side to this question. Albuminuria 
may cause neuritis and not retinitis. It may cause limited 
optic neuritis, in which there may be not only changes in 
the retina that are so slight that you have to look for them 
most closely by the direct method, but in which there may 
be no changes whatever in the retina — a simple optic neu- 
ritis, never anything like so intense as that which is seen 
24 



274 OPTIC NEURITIS. 

here, but which may still be considerable in degree. A 
further inconvenient fact for us, and probably a significant 
one, is that when an isolated optic neuritis is a consequence 
of renal disease, there is generally headache as a very pro- 
nounced symptom, so that the symptoms may be very 
equivocal in character. I remember having this fact im- 
pressed upon me at the beginning of my work with the 
ophthalmoscope in medicine. 

The case was seen when I was a student at University 
College Hospital, and first yielded to the fascination of the 
ophthalmoscope, which was then in its early days as regards 
its application to medicine. The patient suffered from 
severe headache and repeated convulsions. There was 
moderate but distinct optic neuritis, with no change what- 
ever in the retina. I ventured to make a confident diag- 
nosis of cerebral disease, but the post-mortem examination 
showed only granular kidneys. 

The last point of practical importance suggested by the 
case we have considered is this : In the remarkable series 
of surgical operations, which have been done here by Mr. 
Horsley, it has been found that, in cases of intra-cranial 
tumour, and in which nothing could be done to remove 
the tumour, trephining lessened the headache in a remark- 
able degree, and led to rapid subsidence of the optic neu- 
ritis. Special attention has been drawn to this fact by my 
colleague, Dr. James Taylor. This can only be explained 
on the assumption that a causal influence is removed by 
the operation in the diminution of the intra-cranial press- 
ure. The significance of the fact as regards the mecha- 
nism by which optic neuritis is produced may be exagger- 
ated. We know that great excess of intra-cranial pressure 
may exist without optic neuritis. It is probable that its 
influence is to intensify and prolong a neuritis that would 
otherwise be slight and brief.* 

* See, however, added note. 



TREPHINING SUGGESTED. 275 

But this raises the special question — which is, too, a 
somewhat new one — whether an operation in this case 
would be justified in the hope that it might induce a sub- 
sidence of the neuritis and save some sight, apart from any 
attempt to remove the tumour. For the latter purpose the 
question is beset with great difficulties. 

It is one of the cases in which the diagnosis can only be 
carried to a certain point. In the first place, the pain, al- 
though it is to a small extent frontal, is chiefly occipital, 
and has a tendency to pass down the neck. This is gen- 
erally an indication of subtentorial disease. But there is 
also some tenderness above the level of the tentorium on 
percussion of the skull. Percussion of the skull is of some 
use in localising disease. I do not, however, think that we 
have, at present, sufficient grounds to say whether the 
trouble is in the occipital lobe, or whether it may not be 
disease of the cerebellar hemisphere. The tenderness is 
so conspicuously greater on the left side than the right that 
it suggests a unilateral seat of the disease. If it were, in 
the occipital lobe, we should expect to have had a history 
of hemiopia before sight failed. Yet the history does not 
permit us to assume that this was absent because its record 
is absent. In the next place, is there any reason to get at 
the case, excluding glioma and tubercle? If there is a 
family history of phthisis ; if the patient is in the first half 
of life ; if the cause is neither very acute nor very chronic, 
tubercle is most probable. 

In conclusion, I desire to say one word on the practical 
question. Is there any chance of benefit from the operation 
of trephining ? 

The significance of the fact that trephining allows the 
optic neuritis to subside may be easily overrated. It seems 
to show that the increase of intra-cranial pressure is the 
cause. 

To put it shortly, I believe that intra-cranial pressure is a 
factor which intensifies the neuritis ; you see its evidence 



276 OPTIC NEURITIS. 

in the swollen sheath behind the eye in most of these cases. 
But there may be optic neuritis without a swollen sheath,* 
and there may be intra-cranial pressure without optic neu- 
ritis. I remember a case, which shows to how great an 
extent intra-cranial pressure may exist without optic neu- 
ritis. Over the right hemisphere there was growing from 
the dura mater a sarcoma of the size of my fist. The brain 
gave every evidence of compression. The patient had been 
in the hospital, where we had watched her. I was then 
Registrar, and I watched the case afterwards in one of the 
suburbs. The case is fixed in my mind, because I did 
something which afterwards alarmed me. The sun was 
shining in at the window towards which the head of her 
bed was placed. I used the sunlight for the ophthalmo- 
scopic examination, and I was afraid afterwards that the 
concentration of such a powerful light might have blistered 
the retina. But the patient died too soon to permit any 
effect to have been important. 

Intra-cranial pressure, however, may prevent the escape 
of the products of inflammation from the papilla, and per- 
haps may cause additional morbid material to reach the 
papilla from the meninges. It may thus intensify the optic 
neuritis. I will not say that it may not possibly excite it, 
but I believe the chief element of excitation is the passage 
down the nerve of slight interstitial inflammatory changes. 
It is possible that, if there were no increased intra-cranial 
pressure, in a great many cases the optic neuritis thus pro- 
duced would be slight, and perhaps the cases in which 
trephining, by relieving the intra-cranial pressure, allows 
the neuritis to subside, are those in which, without the in- 
creased intra-cranial pressure, the neuritis would already 
have subsided. But any good it can do must depend on 
what capacity for recovery remains in the fibres of the optic 

* See Postscript. 



POSTSCRIPT. 277 

nerve. In optic neuritis the nerve fibres may be damaged 
by propagation to them of inflammation, also by the inter- 
stitial contraction of the products of inflammation when 
these are abundant. At the beginning of subsidence, if 
there is but slight loss of sight, or even if there is none, 
vision may almost entirely fail during the subsidence, in 
consequence of the damage by the contraction of the in- 
flammatory tissue between the fibres. If the neuritis has 
subsided almost to the level of the retina, and there is still 
some sight, it may be improved by the recovery of the 
functional power in fibres which are still continuous, 
although narrowed. But if sight is gone before subsi- 
dence begins, it is certain that the subsidence will complete 
the destruction of any fibres that remain, and no apprecia- 
ble recovery of sight is possible in such cases. 

In our patient there is still in the right eye a little per- 
ception of light, but there is much contraction of tissue 
still to go on, and I think that before that subsidence 
reaches the retina, sight will become extinct. 

Postscript. — The lecture is left as it was delivered, although many 
statements have been contradicted by the later facts of the case. But 
it is often useful thus to perceive such traversing of inference and fact, 
because it discloses the limits of our power of discerning that which 
is, and of forecasting that which is to be. 

After the lecture was delivered, the extensive swelling in the right 
eye lessened with a rapidity that I have never before observed ; a 
difference could be perceived daily, and in a week the swelling was 
not wider than twice the diameter of the disc. The subsidence seems 
to show that the swelling was due to oedema in larger degree than I 
conceived. The part played by oedema has been illustrated in one 
of the microscopical figures in "Medical Ophthalmoscopy," and the 
case gives increased support to Mr. Marcus Gunn's inferences in the 
paper referred to. With this subsidence the headache became much 
less for several days. It then increased to more than its old intensity, 
although the subsidence of the neuritis continued. Trephining, post- 
poned on account of the improvement, became compulsory. It will 
be remembered that the seat of the pain and its passage down the 



278 OPTIC NEURITIS. 

neck, with retraction of the head, pointed to subtentorial disease, but 
the tenderness to percussion was distinctly just above the tentorium 
on the left side. Mr. Horsley trephined below the tentorium at the 
left occipital bone, adopting the method he finds best, first to tre- 
phine, and in a subsequent operation to divide the dura mater. In 
this case he proposed, if he found no subtentorial disease, to divide 
the tentorium and explore above it. After the trephining, before the 
second operation that he intended, the patient died, with general 
convulsions, coma, and respiratory failure. After death an enormous 
cyst was found above the tentorium, in the left occipital lobe. It con- 
tained at least five ounces of clear, pale fluid, and had pushed forward 
the ependyma lining the posterior horn of the lateral ventricle, from 
which it was completely shut off. There were no crystals of any kind 
in the fluid. 

To the eye the cyst seemed simple ; no growth could be discerned. 
But such a simple cyst is almost unknown ; for a simple cyst to cause 
the symptoms of aggressive irritation is, I think, quite unknown. 
Microscopical examination of the wall, by our able pathologist, Dr. 
Colman, showed at one place, at the posterior part of the floor of the 
cyst, distinct evidence of a morbid growth. There was a layer about 
2 mm. thick of sarcomatous tissue, consisting of uniform round cells, 
with abundant embryonic blood-vessels. In several points the growth 
could be seen to be invading the white matter along the lines of the 
vessels. A considerable sized artery in the neighbourhood was com- 
pletely thrombosed, and there was marked hyaline degeneration of 
the blood capillaries in the vicinity of the growth. 

The chief practical lessons the case teaches are these : (i) That 
distinct local tenderness has relatively a very high localising value in 
cortical lesions. (2) That rapid subsidence of an unusually extreme 
swelling of the optic papilla may not have the significance that is pos- 
sessed by slower subsidence of moderate papillitis. Any initial 
hemianopia was not observed, and when the patient came under 
observation sight had failed too much for it to be found. 

Yet one other fact remains to be mentioned, of all, perhaps, the 
most anomalous. If ever the ophthalmoscopic changes suggested 
increased intra-cranial pressure, it was in this case. If ever a morbid 
process seemed capable of causing increase of intra-cranial pressure, 
it was in this case. Yet the condition within the eye, suggestive of 
the cause, subsided rapidly, while the cause remained, as far as could 
be afterwards discerned, unchanged. Lastly, the mechanism by 
which intra-cranial pressure seems to act is considered, on good 
ground, to be always revealed by the distension of the sheath of the 



POSTSCRIPT. 279 

optic nerve behind the eye — enlargement of the space continuous 
with that beneath the arachnoid. In this case there was no disten- 
sion of the sheath, and there was not the least evidence of past dis- 
tension.— W. R. G. 



